Pub Date : 2024-08-01DOI: 10.19852/j.cnki.jtcm.20240515.005
L I Yanjiao, Hao Linyao, L I Shuangyang, Luo Yanqi, Wang Juan, Wang Raoqiong, Bai Xue
Objective: To explore the mechanism by which Tongqiao Yizhi granule (, TQYZKL) intervenes pyroptosis to treat vascular dementia (VaD) in a rat model.
Methods: The rat model of VaD was established by two-vessel occlusion (2VO). The rats were randomly divided into Sham group, Model group, Nimodipine group, TQYZKL (6.2 g?kg-1?d-1), TQYZKL (12.4 g?kg-1?d-1), TQYZKL (24.8 g?kg-1?d-1). The Morris water maze (MWM) test was carried out to test the learning and memory function; Hematoxylin-eosin staining and transmission electron microscopy (TEM) to observe the pathological damage in the hippocampus; Tunel fluorescence staining to detect neuronal pyroptosis in the hippocampus. The expression levels of pyroptosis-related proteins, namely Golgi peripheral membrane protein p65 (P65), nucleotide oligomerization domain-like receptors 3 (NLRP3), caspase-1 and Gasdermin D (GSDMD), were detected using Western blotting and reverse transcription polymerase chain reaction. Moreover, the serum levels of interleukin-1β (IL-1β) and interleukin-18 (IL-18) were determined through the enzyme-linked immunosorbent assay.
Results: The study revealed that TQYZKL effectively improved the ability of VaD ratsto learn and memorize, relieved the pathological damage in the hippocampus, restored neuronal morphology, and reduced the expression of pyroptosis-related proteins P65, NLRP3, caspase-1, GSDMD-N, IL-18 and IL-1β (P < 0.05).
Conclusion: TQYZKL inhibits neuronal pyroptosis in the hippocampus of VaD rats by regulating nuclear factor kappa-B/NLRP3/caspase-1 signaling pathway, thus exerting a therapeutic effect on VaD in the rats.
{"title":"Tongqiao Yizhi granule repress the nuclear factor kappa-b/nucleotide oligomerization domain-like receptors 3/caspase-1 pyroptosis pathway in the hippocampus to counter vascular dementia in rats.","authors":"L I Yanjiao, Hao Linyao, L I Shuangyang, Luo Yanqi, Wang Juan, Wang Raoqiong, Bai Xue","doi":"10.19852/j.cnki.jtcm.20240515.005","DOIUrl":"10.19852/j.cnki.jtcm.20240515.005","url":null,"abstract":"<p><strong>Objective: </strong>To explore the mechanism by which Tongqiao Yizhi granule (, TQYZKL) intervenes pyroptosis to treat vascular dementia (VaD) in a rat model.</p><p><strong>Methods: </strong>The rat model of VaD was established by two-vessel occlusion (2VO). The rats were randomly divided into Sham group, Model group, Nimodipine group, TQYZKL (6.2 g?kg<sup>-1</sup>?d<sup>-1</sup>), TQYZKL (12.4 g?kg<sup>-1</sup>?d<sup>-1</sup>), TQYZKL (24.8 g?kg<sup>-1</sup>?d<sup>-1</sup>). The Morris water maze (MWM) test was carried out to test the learning and memory function; Hematoxylin-eosin staining and transmission electron microscopy (TEM) to observe the pathological damage in the hippocampus; Tunel fluorescence staining to detect neuronal pyroptosis in the hippocampus. The expression levels of pyroptosis-related proteins, namely Golgi peripheral membrane protein p65 (P65), nucleotide oligomerization domain-like receptors 3 (NLRP3), caspase-1 and Gasdermin D (GSDMD), were detected using Western blotting and reverse transcription polymerase chain reaction. Moreover, the serum levels of interleukin-1β (IL-1β) and interleukin-18 (IL-18) were determined through the enzyme-linked immunosorbent assay.</p><p><strong>Results: </strong>The study revealed that TQYZKL effectively improved the ability of VaD ratsto learn and memorize, relieved the pathological damage in the hippocampus, restored neuronal morphology, and reduced the expression of pyroptosis-related proteins P65, NLRP3, caspase-1, GSDMD-N, IL-18 and IL-1β (<i>P</i> < 0.05).</p><p><strong>Conclusion: </strong>TQYZKL inhibits neuronal pyroptosis in the hippocampus of VaD rats by regulating nuclear factor kappa-B/NLRP3/caspase-1 signaling pathway, thus exerting a therapeutic effect on VaD in the rats.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11337261/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141768390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01DOI: 10.19852/j.cnki.jtcm.20240617.001
Zhu Xuan, Lou An, Zhu Keke, Ruan Mingyu
Objective: To investigate the protective effect of the Chinese herbal formula of Jiedu Huayu decoction (, JHD) on oral mucosa of rats with oral submucosal fibrosis (OSF) and its potential mechanism of action.
Methods: Sprague-Dawley male OSF model rats were constructed by injection of betaine and topical rubbing and were randomly grouped and administered by gavage for 4 weeks. Mouth opening and buccal mucosa scores interleukin levels and the expression of Axin and β-catenin proteins or genes were measured before and after drug administration.
Results: After treatment with JHD the buccal mucosal lesions of rats were significantly reduced Axin protein and mRNA expression were significantly increased β-catenin protein and mRNA expression were significantly decreased interleukin-1β and interleukin-6 levels were decreased and interleukin-10 levels were increased.
Conclusion: The mechanism of action of JHD can effectively alleviate the pathological damage of buccal mucosa in OSF rats which may be related to the promotion of Axin expression and inhibition of β-catenin expression.
{"title":"Effect of Jiedu Huayu decoction on oral mucosal Axin and β-catenin expression in oral submucosal fibrosis model rats.","authors":"Zhu Xuan, Lou An, Zhu Keke, Ruan Mingyu","doi":"10.19852/j.cnki.jtcm.20240617.001","DOIUrl":"10.19852/j.cnki.jtcm.20240617.001","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the protective effect of the Chinese herbal formula of Jiedu Huayu decoction (, JHD) on oral mucosa of rats with oral submucosal fibrosis (OSF) and its potential mechanism of action.</p><p><strong>Methods: </strong>Sprague-Dawley male OSF model rats were constructed by injection of betaine and topical rubbing and were randomly grouped and administered by gavage for 4 weeks. Mouth opening and buccal mucosa scores interleukin levels and the expression of Axin and β-catenin proteins or genes were measured before and after drug administration.</p><p><strong>Results: </strong>After treatment with JHD the buccal mucosal lesions of rats were significantly reduced Axin protein and mRNA expression were significantly increased β-catenin protein and mRNA expression were significantly decreased interleukin-1β and interleukin-6 levels were decreased and interleukin-10 levels were increased.</p><p><strong>Conclusion: </strong>The mechanism of action of JHD can effectively alleviate the pathological damage of buccal mucosa in OSF rats which may be related to the promotion of Axin expression and inhibition of β-catenin expression.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11337252/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141768383","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01DOI: 10.19852/j.cnki.jtcm.2024.04.003
Jiang Zhaojian, Cai Hongfei, Yuan Cheng, Cao Lin, X U Wendong, Han Yaming, Zhang Qin, L I Jing, Wang Qin, Liu Juyan
Objective: To investigate the effect of Ganoderma Lucidum Spore Oil (GLSO) on the tumor growth and survival of H22 tumor-bearing mice treated with cyclophosphamide (CTX), and explore the underlying mechanism.
Methods: Allograft H22 hepatocellular carcinoma mouse model was applied to investigate the effect of GLSO on the tumor growth and survival of animals, and Kaplan-Meier survival analysis was used to analyze the life span. Plasma biochemical examination was used to determine the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea (UREA) and creatinine (CRE). Western blot analysis was performed to detect Programmed Death-1 (PD-1), Programmed Death Ligand 1 (PD-L1), Janus Kinase 2 (JAK2), phosphorylated Signal Transducer and Activator of Transcription 3 (p-STAT3), and Signal Transducer and Activator of Transcription 3 (STAT3) expression.
Results: GLSO increased the anti-tumor effect of CTX and prolonged the survival of H22 tumor-bearing mice treated with CTX. Meanwhile, GLSO increased the thymus index and showed no obvious toxicity to liver functions of animals. GLSO also decreased the level of UREA in H22 tumor-bearing mice treated with CTX. Furthermore, GLSO could inhibit the expression of PD-1 in spleen, which was independent of JAK2 expression and STAT3 phosphorylation. However, GLSO did not affect the expression of PD-L1, JAK2, and p-STAT3 in tumor tissue.
Conclusion: GLSO could strengthen the anti-tumor effect of CTX and prolong the life span of H22 tumor-bearing mice, while the underlying mechanism might be relevant to the amelioration effect of thymus function and inhibition of PD-1 expression in spleen. Furthermore, these findings implied the promising role of GLSO in combination with CTX to extend the survival of patients in clinical chemotherapy of hepatocellular carcinoma.
{"title":"Spore Oil enhances the effect of cyclophosphamide inhibiting programmed death-1 and prolongs the survival of H22 tumor-bearing mice.","authors":"Jiang Zhaojian, Cai Hongfei, Yuan Cheng, Cao Lin, X U Wendong, Han Yaming, Zhang Qin, L I Jing, Wang Qin, Liu Juyan","doi":"10.19852/j.cnki.jtcm.2024.04.003","DOIUrl":"10.19852/j.cnki.jtcm.2024.04.003","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the effect of <i>Ganoderma Lucidum</i> Spore Oil (GLSO) on the tumor growth and survival of H22 tumor-bearing mice treated with cyclophosphamide (CTX), and explore the underlying mechanism.</p><p><strong>Methods: </strong>Allograft H22 hepatocellular carcinoma mouse model was applied to investigate the effect of GLSO on the tumor growth and survival of animals, and Kaplan-Meier survival analysis was used to analyze the life span. Plasma biochemical examination was used to determine the levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), urea (UREA) and creatinine (CRE). Western blot analysis was performed to detect Programmed Death-1 (PD-1), Programmed Death Ligand 1 (PD-L1), Janus Kinase 2 (JAK2), phosphorylated Signal Transducer and Activator of Transcription 3 (p-STAT3), and Signal Transducer and Activator of Transcription 3 (STAT3) expression.</p><p><strong>Results: </strong>GLSO increased the anti-tumor effect of CTX and prolonged the survival of H22 tumor-bearing mice treated with CTX. Meanwhile, GLSO increased the thymus index and showed no obvious toxicity to liver functions of animals. GLSO also decreased the level of UREA in H22 tumor-bearing mice treated with CTX. Furthermore, GLSO could inhibit the expression of PD-1 in spleen, which was independent of JAK2 expression and STAT3 phosphorylation. However, GLSO did not affect the expression of PD-L1, JAK2, and p-STAT3 in tumor tissue.</p><p><strong>Conclusion: </strong>GLSO could strengthen the anti-tumor effect of CTX and prolong the life span of H22 tumor-bearing mice, while the underlying mechanism might be relevant to the amelioration effect of thymus function and inhibition of PD-1 expression in spleen. Furthermore, these findings implied the promising role of GLSO in combination with CTX to extend the survival of patients in clinical chemotherapy of hepatocellular carcinoma.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11337259/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141768386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01DOI: 10.19852/j.cnki.jtcm.20240627.001
Zheng Jingrui, Chen Weijian, Y E Binbin, M O Ziyao, D U Qunqun, Qin Renan, Nie Ke
Objective: To determine the therapeutic effects of the Zhuangyao Jianshen pill (, ZYJSP) against benign prostatic hyperplasia (BPH) and investigate the underlying mechanism.
Methods: Forty-eight male Sprague-Dawley rats were randomly divided into six groups: Control group, BPH model group, finasteride-treated group, ZYJSP low, medium and high dose groups. Except for the control group, 40 rats were castrated and injected with testosterone propionate (TP) for 28 consecutive day to induce BPH. Meanwhile, the corresponding drugs were administered by gavage. The prostate wet weight, prostate index (PI), and the histopathological changes in the prostate were measured as the basis for examining the efficacy of ZYJSP against BPH. Levels of the serum sex hormones, oxidative stress markers, inflammatory markers, renal function markers, growth factors, and Cyclin D1 expression in prostate were measured to characterize the therapeutic mechanism of ZYJSP against BPH.
Results: ZYJSP administration significantly reduced prostate wet weight and PI and ameliorated histological changes of the prostate in TP-treated castrated rats. TP markedly increased the levels of creatinine, blood urea nitrogen and growth factors in the serum as well as the expression of the Cyclin D1 in the prostate. Most of these markers were significantly decreased by ZYJSP. ZYJSP significantly restored the dysregulation of testosterone, estradiol, and dihydrotestosterone caused by TP. Furthermore, ZYJSP relieved TP-induced prostate injury and exhibited both anti-inflammatory and anti-oxidant activity by decreasing interleukin-6, interleukin-8, and malondialdehyde levels and increasing the activity of superoxide dismutase in the serum.
Conclusion: These findings indicate that ZYJSP can effectively ameliorate BPH induced by TP in castrated rats, and the underlying mechanism might be related to regulating sex hormone balance, reducing oxidative stress, and inhibiting the inflammatory response.
{"title":"Zhuangyao Jianshen pill ameliorates testosterone-induced benign postatic hyperplasia in rats.","authors":"Zheng Jingrui, Chen Weijian, Y E Binbin, M O Ziyao, D U Qunqun, Qin Renan, Nie Ke","doi":"10.19852/j.cnki.jtcm.20240627.001","DOIUrl":"10.19852/j.cnki.jtcm.20240627.001","url":null,"abstract":"<p><strong>Objective: </strong>To determine the therapeutic effects of the Zhuangyao Jianshen pill (, ZYJSP) against benign prostatic hyperplasia (BPH) and investigate the underlying mechanism.</p><p><strong>Methods: </strong>Forty-eight male Sprague-Dawley rats were randomly divided into six groups: Control group, BPH model group, finasteride-treated group, ZYJSP low, medium and high dose groups. Except for the control group, 40 rats were castrated and injected with testosterone propionate (TP) for 28 consecutive day to induce BPH. Meanwhile, the corresponding drugs were administered by gavage. The prostate wet weight, prostate index (PI), and the histopathological changes in the prostate were measured as the basis for examining the efficacy of ZYJSP against BPH. Levels of the serum sex hormones, oxidative stress markers, inflammatory markers, renal function markers, growth factors, and Cyclin D1 expression in prostate were measured to characterize the therapeutic mechanism of ZYJSP against BPH.</p><p><strong>Results: </strong>ZYJSP administration significantly reduced prostate wet weight and PI and ameliorated histological changes of the prostate in TP-treated castrated rats. TP markedly increased the levels of creatinine, blood urea nitrogen and growth factors in the serum as well as the expression of the Cyclin D1 in the prostate. Most of these markers were significantly decreased by ZYJSP. ZYJSP significantly restored the dysregulation of testosterone, estradiol, and dihydrotestosterone caused by TP. Furthermore, ZYJSP relieved TP-induced prostate injury and exhibited both anti-inflammatory and anti-oxidant activity by decreasing interleukin-6, interleukin-8, and malondialdehyde levels and increasing the activity of superoxide dismutase in the serum.</p><p><strong>Conclusion: </strong>These findings indicate that ZYJSP can effectively ameliorate BPH induced by TP in castrated rats, and the underlying mechanism might be related to regulating sex hormone balance, reducing oxidative stress, and inhibiting the inflammatory response.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11337254/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141768393","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01DOI: 10.19852/j.cnki.jtcm.20240626.002
Liu Tongtong, Zhang Xi, Yang Hui, Lin Xiaoyuan, Liu Jian, Zhang Xiuli, Guo Dongwei, Zhao Hongqing, Zou Manshu, Lei Chang, Long Hongping, Luo Yan, Xiang Yun, G E Jinwen, Wang Yuhong, Meng Pan
Objective: To investigate the effects of luteolin on chronic unpredictable mild stress (CUMS)-induced depressive rats and corticosterone (CORT)-induced depressive primary hippocampal neurons, and to elucidate the mechanism behind the action.
Methods: The antidepressant mechanism of luteolin was studied by using CUMS rat model and primary hippocampal neurons in fetal rats. In vivo, novelty suppressed feeding, open-field and sucrose preference tests as well as Morris water maze were evaluated. The content of brain derived neurotrophic factor (BDNF), 5-hydroxytryptamine (5-HT), norepinephrine (NE), and dopamine (DA) in serum were detected by enzyme-linked immunosorbent assay. The mechanisms of luteolin were explored based on neurotrophin and hippocampal neurogenesis, and proliferation. Survival of the septo-temporal axis in hippocampus was assayed using the 5-bromo-2-deoxyuridine (BrdU), the expression of BDNF, neurotrophin-3 (NT-3), and nerve growth factor (NGF) in hippocampus dentate gyrus region were measured by Western-blotting. In vitro, BDNF, NT-3, tropomyosin receptor kinase B (TrkB), and phosphorylated cyclic adenosine monophosphate responsive element binding protein (p-CREB) were detected through the high content analysis (HCA) to investigate neurotrophin and apoptosis.
Results: Induction of CUMS in rats induced depressive symptoms, while luteolin significantly enhanced sucrose consumption, decreased feeding latency, increased locomotor activity, escape latency, distance of target quadrant and regulated the content of depressive-like biomarkers. Histology analysis revealed that luteolin increased the abundance of new born neurons that had been labeled with BrdU, BrdU + neuronal nuclear antigen, and BrdU + doublecortin in septo-temporal axis of S2 (mid-septal) and T3 (mid-temporal). Moreover, expression of BDNF, NT-3, and NGF increased significantly in the septo-temporal axis of S2 and T3. HCA showed increased expression of BDNF, NT-3, TrkB and p-CREB in primary hippocampal neurons.
Conclusion: The results provided direct evidence that luteolin has an antidepressant effect and could effectively promote the regeneration of the septotemporal axis nerve and hippocampal neuronutrition, which suggested that the antidepressant effect of luteolin may be related to hippocampal neurogenesis.
研究目的研究叶黄素对慢性不可预知温和应激(CUMS)诱导的抑郁大鼠和皮质酮(CORT)诱导的抑郁性原发性海马神经元的影响,并阐明其作用机制:方法:利用CUMS大鼠模型和胎鼠原发性海马神经元研究了木犀草素的抗抑郁机制。方法:利用 CUMS 大鼠模型和胎鼠海马原代神经元研究了木犀草素的抗抑郁机制。通过酶联免疫吸附试验检测了血清中脑源性神经营养因子(BDNF)、5-羟色胺(5-HT)、去甲肾上腺素(NE)和多巴胺(DA)的含量。研究人员从神经营养素、海马神经发生和增殖的角度探讨了木犀草素的作用机制。用5-溴-2-脱氧尿苷(BrdU)检测了海马隔颞轴的存活率,用Western-印迹法测定了海马齿状回区BDNF、神经营养素-3(NT-3)和神经生长因子(NGF)的表达。在体外,通过高含量分析(HCA)检测BDNF、NT-3、肌钙蛋白受体激酶B(TrkB)和磷酸化环磷酸腺苷单磷酸反应元件结合蛋白(p-CREB),以研究神经营养素和细胞凋亡:结果:诱导CUMS大鼠可诱发抑郁症状,而叶黄素可显著提高蔗糖消耗量,降低摄食潜伏期,提高运动活性、逃逸潜伏期、目标象限距离,并调节抑郁样生物标志物的含量。组织学分析表明,叶黄素增加了S2(中隔)和T3(中颞)中隔-颞轴上用BrdU、BrdU+神经元核抗原和BrdU+双皮质素标记的新生神经元的数量。此外,BDNF、NT-3 和 NGF 的表达在 S2 和 T3 的颞中轴显著增加。HCA显示原发性海马神经元中BDNF、NT-3、TrkB和p-CREB的表达增加:研究结果提供了叶黄素具有抗抑郁作用的直接证据,并能有效促进颞中轴神经和海马神经营养的再生,这表明叶黄素的抗抑郁作用可能与海马神经发生有关。
{"title":"Luteolin promotes neuronogenesis in hippocampus of chronic unpredictable mild stress rats and primary hippocampus of fetal rats.","authors":"Liu Tongtong, Zhang Xi, Yang Hui, Lin Xiaoyuan, Liu Jian, Zhang Xiuli, Guo Dongwei, Zhao Hongqing, Zou Manshu, Lei Chang, Long Hongping, Luo Yan, Xiang Yun, G E Jinwen, Wang Yuhong, Meng Pan","doi":"10.19852/j.cnki.jtcm.20240626.002","DOIUrl":"10.19852/j.cnki.jtcm.20240626.002","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the effects of luteolin on chronic unpredictable mild stress (CUMS)-induced depressive rats and corticosterone (CORT)-induced depressive primary hippocampal neurons, and to elucidate the mechanism behind the action.</p><p><strong>Methods: </strong>The antidepressant mechanism of luteolin was studied by using CUMS rat model and primary hippocampal neurons in fetal rats. <i>In vivo</i>, novelty suppressed feeding, open-field and sucrose preference tests as well as Morris water maze were evaluated. The content of brain derived neurotrophic factor (BDNF), 5-hydroxytryptamine (5-HT), norepinephrine (NE), and dopamine (DA) in serum were detected by enzyme-linked immunosorbent assay. The mechanisms of luteolin were explored based on neurotrophin and hippocampal neurogenesis, and proliferation. Survival of the septo-temporal axis in hippocampus was assayed using the 5-bromo-2-deoxyuridine (BrdU), the expression of BDNF, neurotrophin-3 (NT-3), and nerve growth factor (NGF) in hippocampus dentate gyrus region were measured by Western-blotting. <i>In vitro</i>, BDNF, NT-3, tropomyosin receptor kinase B (TrkB), and phosphorylated cyclic adenosine monophosphate responsive element binding protein (p-CREB) were detected through the high content analysis (HCA) to investigate neurotrophin and apoptosis.</p><p><strong>Results: </strong>Induction of CUMS in rats induced depressive symptoms, while luteolin significantly enhanced sucrose consumption, decreased feeding latency, increased locomotor activity, escape latency, distance of target quadrant and regulated the content of depressive-like biomarkers. Histology analysis revealed that luteolin increased the abundance of new born neurons that had been labeled with BrdU, BrdU + neuronal nuclear antigen, and BrdU + doublecortin in septo-temporal axis of S2 (mid-septal) and T3 (mid-temporal). Moreover, expression of BDNF, NT-3, and NGF increased significantly in the septo-temporal axis of S2 and T3. HCA showed increased expression of BDNF, NT-3, TrkB and p-CREB in primary hippocampal neurons.</p><p><strong>Conclusion: </strong>The results provided direct evidence that luteolin has an antidepressant effect and could effectively promote the regeneration of the septotemporal axis nerve and hippocampal neuronutrition, which suggested that the antidepressant effect of luteolin may be related to hippocampal neurogenesis.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11337264/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141768333","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01DOI: 10.19852/j.cnki.jtcm.20240626.003
L I Zhongzheng, Zhao Yadan, Ma Weigang, Zhang Yonglong, X U Zhifang, X I Qiang, L I Yanqi, Qin Siru, Zhang Zichen, Wang Songtao, Zhao Xue, Liu Yangyang, Guo Yi, Guo Yongming
Objective: To investigate the mechanisms behind the effects of acupuncture in Traditional Chinese Medicine, we delved into the adenosine triphosphate/peripheral purinergic P2X receptor 3 (ATP/P2X3) receptor signaling system as an indicator of the body's energy state, commonly referred to as "Qi".
Methods: The tail-flick test was utilized to explore the impact of acupuncture on pain tolerance threshold (PTT) in mice, while also assessing adenosine (ADO) levels and adenylate energy charge (EC) at Zusanli (ST36). The study further investigated the dose-dependent effects of acupuncture on PTT and ADO levels at Zusanli (ST36). To shed light on the underlying mechanisms of acupuncture's effects, the study examined the impact of ATP, a P2X3 receptor antagonist, and adenosine disodium on PTT following acupuncture administration.
Results: Acupuncture at Zusanli (ST36) led to significant improvements in PTT in mice, with the most effective interventions being twirling for 2 min and needle retention for 28 min. These interventions also resulted in significant increases in ATP levels. The effects of acupuncture were further augmented by administration of different doses of ATP at Zusanli (ST36), and pretreatment with a P2X3 receptor antagonist decreased PTT. Adenylate EC peaked at 30 min after intraperitoneal injection of ATP, and pretreatment with various doses of i.p. ATP 30 min prior to acupuncture increased PTT in a dose-dependent manner. Additionally, pretreatment with an i.p. or intramuscular injection of adenosine disodium enhanced the effects of acupuncture.
Conclusion: This research provides compelling evidence that ATP is involved in the regulation of PTT through acupuncture, revealing new avenues for achieving enhanced clinical outcomes.
研究目的为了研究中医针灸的作用机制,我们深入研究了作为人体能量状态指标的三磷酸腺苷/外周嘌呤能P2X受体3(ATP/P2X3)信号系统:方法:本研究利用尾闪试验来探讨针灸对小鼠疼痛耐受阈值(PTT)的影响,同时还评估了祖三里(ST36)的腺苷(ADO)水平和腺苷酸能量电荷(EC)。研究进一步探讨了针灸对小鼠疼痛阈值(PTT)和足三里(ST36)腺苷(ADO)水平的剂量依赖性影响。为了揭示针灸作用的内在机制,研究还考察了P2X3受体拮抗剂ATP和腺苷二钠对针刺后PTT的影响:结果:针刺足三里(ST36)可显著改善小鼠的 PTT,最有效的干预措施是捻转 2 分钟和留针 28 分钟。这些干预措施还能显著提高 ATP 水平。在足三里(ST36)注射不同剂量的 ATP 可进一步增强针灸的效果,而使用 P2X3 受体拮抗剂可降低 PTT。腹腔注射 ATP 后 30 分钟腺苷酸 EC 达到峰值,针刺前 30 分钟给予不同剂量的静注 ATP 会以剂量依赖的方式增加 PTT。此外,腹腔注射或肌肉注射腺苷二钠可增强针灸的效果:这项研究提供了令人信服的证据,证明 ATP 参与了针灸对 PTT 的调节,为提高临床疗效提供了新的途径。
{"title":"Adenosine triphosphate mediates the pain tolerance effect of manual acupuncture at Zusanli (ST36) in mice.","authors":"L I Zhongzheng, Zhao Yadan, Ma Weigang, Zhang Yonglong, X U Zhifang, X I Qiang, L I Yanqi, Qin Siru, Zhang Zichen, Wang Songtao, Zhao Xue, Liu Yangyang, Guo Yi, Guo Yongming","doi":"10.19852/j.cnki.jtcm.20240626.003","DOIUrl":"10.19852/j.cnki.jtcm.20240626.003","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the mechanisms behind the effects of acupuncture in Traditional Chinese Medicine, we delved into the adenosine triphosphate/peripheral purinergic P2X receptor 3 (ATP/P2X3) receptor signaling system as an indicator of the body's energy state, commonly referred to as \"<i>Qi</i>\".</p><p><strong>Methods: </strong>The tail-flick test was utilized to explore the impact of acupuncture on pain tolerance threshold (PTT) in mice, while also assessing adenosine (ADO) levels and adenylate energy charge (EC) at Zusanli (ST36). The study further investigated the dose-dependent effects of acupuncture on PTT and ADO levels at Zusanli (ST36). To shed light on the underlying mechanisms of acupuncture's effects, the study examined the impact of ATP, a P2X3 receptor antagonist, and adenosine disodium on PTT following acupuncture administration.</p><p><strong>Results: </strong>Acupuncture at Zusanli (ST36) led to significant improvements in PTT in mice, with the most effective interventions being twirling for 2 min and needle retention for 28 min. These interventions also resulted in significant increases in ATP levels. The effects of acupuncture were further augmented by administration of different doses of ATP at Zusanli (ST36), and pretreatment with a P2X3 receptor antagonist decreased PTT. Adenylate EC peaked at 30 min after intraperitoneal injection of ATP, and pretreatment with various doses of i.p. ATP 30 min prior to acupuncture increased PTT in a dose-dependent manner. Additionally, pretreatment with an i.p. or intramuscular injection of adenosine disodium enhanced the effects of acupuncture.</p><p><strong>Conclusion: </strong>This research provides compelling evidence that ATP is involved in the regulation of PTT through acupuncture, revealing new avenues for achieving enhanced clinical outcomes.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11337262/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141768381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01DOI: 10.19852/j.cnki.jtcm.20240610.003
Guo Yanding, Luo Kun, Zhang Linlin, L U Wenting, Shang Yanan, Zhong Yumei, H U Danhui, Yang Xin, Zhou Haiyan
Objective: To determine whether moxibustion had an anti-inflammatory effect on rheumatoid arthritis (RA) by regulating Annexin 1 expression and interfering with the phospholipaseA2 signaling pathway.
Methods: Thirty male Sprague-Dawley rats were randomly categorized into five groups (six rats per group): blank control (CON) group, RA model (RA) group, moxibustion (MOX) group, Annexin 1 lentiviral intervention (RNAi-Anxa1) group, and Annexin 1 lentiviral intervention + moxibustion (RNAi-Anxa1 + MOX) group. The rats in the RNAi-Anxa1 and the RNAi-Anxa1 + MOX groups were injected with the lentiviral vector-mediated RNAi-Anxa1 into the rat foot pad. An experimental RA rat model was established by injecting Freund's complete adjuvant (FCA) into the RA, MOX, RNAi-Anxa1, and RNAi-Anxa1 + MOX groups. Rats in the MOX and RNAi-Anxa1 + MOX groups received moxibustion treatment. After modeling, using moxibustion "Shenshu (BL23)" and "Zusanli (ST36)", each point is 5 times, bilateral alternating, once a day, 6 times for a course of treatment, between the courses of rest for a one day. A total of three treatment courses were conducted. Both bilateral pad thicknesses were measured using Vernier calipers on experimental days 1, 7, 14, 21, and 28. The expression of cPLA2α signaling in the synovium of diseased joints was observed using Western blot. The pathology of the rat ankle synovium was observed using hematoxylin-eosin (HE) staining. Interleukin (IL)-1β, IL-10, prostaglandin E2 (PGE2), and leukotriene B4 (LTB4) were detected using enzyme-linked immunosorbent assay.
Results: Moxibustion increased the levels of Annexin 1 and decreased the inflammatory response in rats with RA. After increasing the expression of Annexin 1, the phosphorylated expression of cPLA2α was inhibited, the serum levels of IL-1β, PGE2, and LTB4 decreased, and the level of IL-10 increased. In moxibustion treated RA rats after the Annexin 1 lentiviral intervention, the serum levels of IL-1β, PGE2, LTB4, and IL-10 were almost unchanged.
Conclusion: Moxibustion enhanced the negative regulation of the cPLA2α signaling pathway, increased the synovial Annexin 1 expression, inhibited the cPLA2α signaling pathway, indirectly inhibited the expression of downstream inflammatory factors, and played a role in reducing inflammation.
{"title":"Study on the anti-inflammatory mechanism of moxibustion in rheumatoid arthritis in rats based on phospholipaseA2 signaling inhibition by Annexin 1.","authors":"Guo Yanding, Luo Kun, Zhang Linlin, L U Wenting, Shang Yanan, Zhong Yumei, H U Danhui, Yang Xin, Zhou Haiyan","doi":"10.19852/j.cnki.jtcm.20240610.003","DOIUrl":"10.19852/j.cnki.jtcm.20240610.003","url":null,"abstract":"<p><strong>Objective: </strong>To determine whether moxibustion had an anti-inflammatory effect on rheumatoid arthritis (RA) by regulating Annexin 1 expression and interfering with the phospholipaseA2 signaling pathway.</p><p><strong>Methods: </strong>Thirty male Sprague-Dawley rats were randomly categorized into five groups (six rats per group): blank control (CON) group, RA model (RA) group, moxibustion (MOX) group, Annexin 1 lentiviral intervention (RNAi-Anxa1) group, and Annexin 1 lentiviral intervention + moxibustion (RNAi-Anxa1 + MOX) group. The rats in the RNAi-Anxa1 and the RNAi-Anxa1 + MOX groups were injected with the lentiviral vector-mediated RNAi-Anxa1 into the rat foot pad. An experimental RA rat model was established by injecting Freund's complete adjuvant (FCA) into the RA, MOX, RNAi-Anxa1, and RNAi-Anxa1 + MOX groups. Rats in the MOX and RNAi-Anxa1 + MOX groups received moxibustion treatment. After modeling, using moxibustion \"Shenshu (BL23)\" and \"Zusanli (ST36)\", each point is 5 times, bilateral alternating, once a day, 6 times for a course of treatment, between the courses of rest for a one day. A total of three treatment courses were conducted. Both bilateral pad thicknesses were measured using Vernier calipers on experimental days 1, 7, 14, 21, and 28. The expression of cPLA2α signaling in the synovium of diseased joints was observed using Western blot. The pathology of the rat ankle synovium was observed using hematoxylin-eosin (HE) staining. Interleukin (IL)-1β, IL-10, prostaglandin E2 (PGE2), and leukotriene B4 (LTB4) were detected using enzyme-linked immunosorbent assay.</p><p><strong>Results: </strong>Moxibustion increased the levels of Annexin 1 and decreased the inflammatory response in rats with RA. After increasing the expression of Annexin 1, the phosphorylated expression of cPLA2α was inhibited, the serum levels of IL-1β, PGE2, and LTB4 decreased, and the level of IL-10 increased. In moxibustion treated RA rats after the Annexin 1 lentiviral intervention, the serum levels of IL-1β, PGE2, LTB4, and IL-10 were almost unchanged.</p><p><strong>Conclusion: </strong>Moxibustion enhanced the negative regulation of the cPLA2α signaling pathway, increased the synovial Annexin 1 expression, inhibited the cPLA2α signaling pathway, indirectly inhibited the expression of downstream inflammatory factors, and played a role in reducing inflammation.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11337253/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141768387","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01DOI: 10.19852/j.cnki.jtcm.2024.04.005
Yao Yuning, Cao Kegang, Zhang Genming, Liu Jianping, Chen Wei, Cao Junling, Yang Wenming, Yan Yongmei, Geng Chang, J U Yi, Zhao Dexi, Q U Mia, L I Xiaoli, Sun Li, Han Zhenyun, H E Liyun, Cui Fangyuan, F U Caihong, Zhou Bo, Liao Shuqin
Objective: To summarize the evidence from Traditional Chinese Medicine (TCM) practice in the treatment of acute primary headache and provide clinical practice guidance.
Methods: The guidelines were developed in accordance with the World Health Organization guideline development manual. After the establishment of steering committee, panel and the registration and protocol formulation, the evidence on TCM for acute primary headache from published guidelines, clinical evidence, and expert experience and consensus were collected. The grading of recommendations assessment, development and evaluation method was used to grade the evidence and make the recommendations.
Results: Based on the available evidence, the guidelines recommended three TCM herbal decoctions, six Chinese patent medicines, and two kinds of external application of Chinese herbal medicines. Diagnostic recommendations based on the expert experience and consensus were also included in the guidelines.
Conclusion: TCM diagnosis and treatment of decoction, Chinese patent medicine and external application for treating acute primary headache were recommended. We hope these guidelines will be helpful in standardize the TCM acute treatment of primary headache.
{"title":"International standard of Traditional Chinese Medicine Techniques: Traditional Chinese Medicine guidelines for acute primary headache (2022).","authors":"Yao Yuning, Cao Kegang, Zhang Genming, Liu Jianping, Chen Wei, Cao Junling, Yang Wenming, Yan Yongmei, Geng Chang, J U Yi, Zhao Dexi, Q U Mia, L I Xiaoli, Sun Li, Han Zhenyun, H E Liyun, Cui Fangyuan, F U Caihong, Zhou Bo, Liao Shuqin","doi":"10.19852/j.cnki.jtcm.2024.04.005","DOIUrl":"10.19852/j.cnki.jtcm.2024.04.005","url":null,"abstract":"<p><strong>Objective: </strong>To summarize the evidence from Traditional Chinese Medicine (TCM) practice in the treatment of acute primary headache and provide clinical practice guidance.</p><p><strong>Methods: </strong>The guidelines were developed in accordance with the World Health Organization guideline development manual. After the establishment of steering committee, panel and the registration and protocol formulation, the evidence on TCM for acute primary headache from published guidelines, clinical evidence, and expert experience and consensus were collected. The grading of recommendations assessment, development and evaluation method was used to grade the evidence and make the recommendations.</p><p><strong>Results: </strong>Based on the available evidence, the guidelines recommended three TCM herbal decoctions, six Chinese patent medicines, and two kinds of external application of Chinese herbal medicines. Diagnostic recommendations based on the expert experience and consensus were also included in the guidelines.</p><p><strong>Conclusion: </strong>TCM diagnosis and treatment of decoction, Chinese patent medicine and external application for treating acute primary headache were recommended. We hope these guidelines will be helpful in standardize the TCM acute treatment of primary headache.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11337266/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141768332","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01DOI: 10.19852/j.cnki.jtcm.20240515.002
W U Zhiwei, Zhu Qingguang, Kong Lingjun, Song Pengfei, Zhou Xin, Guo Guangxin, Zhang Shuaipan, H E Tianxiang, Cheng Yanbin, Fang Min
Objective: To observe the analgesic effects of Tuina on neuropathic pain (NPP) and the underlying mechanisms.
Methods: Forty-eight Sprague-Dawley (SD) rats were assigned by random into three treatment groups: sham, chronic constriction injury (CCI), and Tuina. Each group contained sixteen rats. CCI model was generated by ligating the right sciatic nerve. Behavioral changes of CCI were assessed by the paw withdrawal threshold (PWT) and paw withdrawal latency (PWL). In addition, biochemical techniques such as immunofluorescence staining, enzyme-linked immunosorbent assay (ELISA) and Western blotting were used to profile levels of microglia activation and inflammatory factors in the spinal dorsal horn (SDH) of rats. Tuina (clockwise pressing and rubbing) was performed at Chengshan (BL57) to observe the analgesic effects on CCI rats and the underlying mechanisms.
Results: Rats with CCI experienced significant reduction in the PWT and PWL of the right hind paw relative to CCI group at day 3. Tuina treatment rescued this situation significantly on days 10 and 14. Besides, Iba-1, microglia M1 receptor CD68, tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) were higher in the right SDH for CCI group compared to the sham group on day 14. As expected, Tuina partially downregulated the CCI-induced overexpressed Iba-1, CD68, TNF-α, and IL-1β in the SDH of CCI model.
Conclusion: Tuina induces a time-dependent cumulative analgesic effect in CCI rats by inhibiting the activation of microglia and the secretion of IL-1β and TNF-α in SDH.
{"title":"Tuina alleviates neuropathic pain through regulate the activation of microglia and the secretion of inflammatory cytokine in spinal cord.","authors":"W U Zhiwei, Zhu Qingguang, Kong Lingjun, Song Pengfei, Zhou Xin, Guo Guangxin, Zhang Shuaipan, H E Tianxiang, Cheng Yanbin, Fang Min","doi":"10.19852/j.cnki.jtcm.20240515.002","DOIUrl":"10.19852/j.cnki.jtcm.20240515.002","url":null,"abstract":"<p><strong>Objective: </strong>To observe the analgesic effects of Tuina on neuropathic pain (NPP) and the underlying mechanisms.</p><p><strong>Methods: </strong>Forty-eight Sprague-Dawley (SD) rats were assigned by random into three treatment groups: sham, chronic constriction injury (CCI), and Tuina. Each group contained sixteen rats. CCI model was generated by ligating the right sciatic nerve. Behavioral changes of CCI were assessed by the paw withdrawal threshold (PWT) and paw withdrawal latency (PWL). In addition, biochemical techniques such as immunofluorescence staining, enzyme-linked immunosorbent assay (ELISA) and Western blotting were used to profile levels of microglia activation and inflammatory factors in the spinal dorsal horn (SDH) of rats. Tuina (clockwise pressing and rubbing) was performed at Chengshan (BL57) to observe the analgesic effects on CCI rats and the underlying mechanisms.</p><p><strong>Results: </strong>Rats with CCI experienced significant reduction in the PWT and PWL of the right hind paw relative to CCI group at day 3. Tuina treatment rescued this situation significantly on days 10 and 14. Besides, Iba-1, microglia M1 receptor CD68, tumor necrosis factor-α (TNF-α), and interleukin-1β (IL-1β) were higher in the right SDH for CCI group compared to the sham group on day 14. As expected, Tuina partially downregulated the CCI-induced overexpressed Iba-1, CD68, TNF-α, and IL-1β in the SDH of CCI model.</p><p><strong>Conclusion: </strong>Tuina induces a time-dependent cumulative analgesic effect in CCI rats by inhibiting the activation of microglia and the secretion of IL-1β and TNF-α in SDH.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11337246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141768391","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-01DOI: 10.19852/j.cnki.jtcm.20240610.005
H U Yuanyuan, Liu Xinguang, Zhao Peng, W U Jinyan, Yan Xinhua, Hou Runsu, Wang Xiangcheng, Yang Fan, Tian Xinrong, L I Jiansheng
Objective: To explore the mechanisms of Yangqing Chenfei formula (, YCF) in the treatment of silicosis through a comprehensive strategy consisting of serum pharmacochemistry, network pharmacology analysis, and in vitro validation.
Methods: An ultrahigh-performance liquid chroma-tography-tandem mass spectrometry method was used to confirm the active components in YCF-medicated serum. Then, we obtained targets for active components and genes for silicosis from multiple databases. Furthermore, a protein-protein interaction network was constructed, and Kyoto Encyclopedia of Genes and Genomes pathway and biological process analyses were conducted to elucidate the mechanisms of YCF for the treatment of silicosis. Finally, we validated the important components and mechanisms in vitro.
Results: Altogether, 19 active components were identified from rat serum after YCF administration. We identified 724 targets for 19 components, which were mainly related to inflammation [phosphatidy linositol 3 kinase/protein kinase B, forkhead box O, hypoxia inducible factor, and T-cell receptor signaling pathway, nitric oxide biosynthetic process], fibrotic processes [vascular endothelial growth factor signaling pathway, extracellular signal regulated kinase (ERK) 1 and ERK2 cascade, smooth muscle cell proliferation], and apoptosis (negative regulation of apoptotic process). In addition, 218 genes for silicosis were identified and were mainly associated with the inflammatory response and immune process [cytokine?cytokine receptor interaction, tumor necrosis factor alpha (TNF-α), toll-like receptor, and nucleotide binding oligomerization domain-like receptor signaling pathway]. Taking an intersection of active component targets and silicosis genes, we obtained 61 common genes that were mainly related to the inflammatory response and apoptosis, such as the phosphatidylinositol-3-kinase/protein kinase B signaling pathway, mitogen activated protein kinases signaling pathway, TNF signaling pathway, toll-like receptor signaling pathway, biosynthesis of nitric oxide, and apoptotic process. In the herb-component-gene-pathway network, paeoniflorin, rutin and nobiletin targeted the most genes. In vitro, paeoniflorin, rutin and nobiletin decreased the mRNA levels of inflammatory factors [interleukin (IL)-6, TNF-α, and IL-1β], suppressed p-AKT and cleaved caspase-3, and increased B cell lymphoma (Bcl)-2 protein expression in silica-induced macrophages in a concentration-dependent manner.
Conclusion: YCF could significantly relieve the inflammatory response of silicosis via suppression of the AKT/Bcl-2/Caspase-3 pathway.
{"title":"Integration of serum pharmacochemistry with network pharmacology to reveal the potential mechanism of Yangqing Chenfei formula for the treatment of silicosis.","authors":"H U Yuanyuan, Liu Xinguang, Zhao Peng, W U Jinyan, Yan Xinhua, Hou Runsu, Wang Xiangcheng, Yang Fan, Tian Xinrong, L I Jiansheng","doi":"10.19852/j.cnki.jtcm.20240610.005","DOIUrl":"10.19852/j.cnki.jtcm.20240610.005","url":null,"abstract":"<p><strong>Objective: </strong>To explore the mechanisms of Yangqing Chenfei formula (, YCF) in the treatment of silicosis through a comprehensive strategy consisting of serum pharmacochemistry, network pharmacology analysis, and <i>in vitro</i> validation.</p><p><strong>Methods: </strong>An ultrahigh-performance liquid chroma-tography-tandem mass spectrometry method was used to confirm the active components in YCF-medicated serum. Then, we obtained targets for active components and genes for silicosis from multiple databases. Furthermore, a protein-protein interaction network was constructed, and Kyoto Encyclopedia of Genes and Genomes pathway and biological process analyses were conducted to elucidate the mechanisms of YCF for the treatment of silicosis. Finally, we validated the important components and mechanisms <i>in vitro</i>.</p><p><strong>Results: </strong>Altogether, 19 active components were identified from rat serum after YCF administration. We identified 724 targets for 19 components, which were mainly related to inflammation [phosphatidy linositol 3 kinase/protein kinase B, forkhead box O, hypoxia inducible factor, and T-cell receptor signaling pathway, nitric oxide biosynthetic process], fibrotic processes [vascular endothelial growth factor signaling pathway, extracellular signal regulated kinase (ERK) 1 and ERK2 cascade, smooth muscle cell proliferation], and apoptosis (negative regulation of apoptotic process). In addition, 218 genes for silicosis were identified and were mainly associated with the inflammatory response and immune process [cytokine?cytokine receptor interaction, tumor necrosis factor alpha (TNF-α), toll-like receptor, and nucleotide binding oligomerization domain-like receptor signaling pathway]. Taking an intersection of active component targets and silicosis genes, we obtained 61 common genes that were mainly related to the inflammatory response and apoptosis, such as the phosphatidylinositol-3-kinase/protein kinase B signaling pathway, mitogen activated protein kinases signaling pathway, TNF signaling pathway, toll-like receptor signaling pathway, biosynthesis of nitric oxide, and apoptotic process. In the herb-component-gene-pathway network, paeoniflorin, rutin and nobiletin targeted the most genes. <i>In vitro</i>, paeoniflorin, rutin and nobiletin decreased the mRNA levels of inflammatory factors [interleukin (IL)-6, TNF-α, and IL-1β], suppressed p-AKT and cleaved caspase-3, and increased B cell lymphoma (Bcl)-2 protein expression in silica-induced macrophages in a concentration-dependent manner.</p><p><strong>Conclusion: </strong>YCF could significantly relieve the inflammatory response of silicosis <i>via</i> suppression of the AKT/Bcl-2/Caspase-3 pathway.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11337247/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141768330","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}