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Actinidia chinensis polysaccharide interferes with the epithelial-mesenchymal transition of gastric cancer by regulating the nuclear transcription factor-κB pathway to inhibit invasion and metastasis. 放线菌多糖通过调节核转录因子-κB通路干扰胃癌的上皮-间质转化,从而抑制侵袭和转移。
Pub Date : 2024-10-01 DOI: 10.19852/j.cnki.jtcm.20240806.001
Zhang Guangshun, X U Xiaonan, X U Chuyun, Liao Guanghui, X U Hao, Lou Zhaohuan, Zhang Guangji

Objective: To investigate the mechanisms of the effect of Actinidia chinensis polysaccharide (ACPS) on the invasion and metastasis of gastric cancer cells.

Methods: BGC-823-Luc gastric cancer cells stably transfected with a luciferase gene were used to establish an insitutransplanted tumor mouse model. A live mouse imaging system was used to observe tumor growth, and hematoxylin and eosin staining was applied to analyze tissue histopathology. Transwell and scratch wound assays were performed to examine the invasive and migratory ability of BGC-823 cells. Immunofluorescence, confocal microscopy, immunohistochemistry, and Western blot assays were used to analyze the expressions of the nuclear transcription factor-κB (NF-κB) signaling pathway and epithelial-mesenchymal transition (EMT)-related proteins.

Results: ACPS significantly inhibited the growth of subcutaneously transplanted BGC-823-Luc gastric cancer tumors in nude mice and reduced inflammatory cell infiltration in tumor tissues. ACPS inhibited Epidermal Growth Factor-induced invasion, migration, and morphological changes in the cytoskeleton of BGC-823 cells. ACPS inhibited gastric cancer EMT and decreased the expression of matrix metallopeptidase 9, N-cadherin and p-NF-κB p65 in transplanted tumor tissues. ACPS inhibited the expression of matrix metalloproteinases and vascular adhesion factors in BGC-823 cells, promoted p65-NF-κB nuclear translocation, and regulated proteins associated with the NF-κB p65 pathway.

Conclusions: ACPS inhibited gastric cancer invasion and metastasis both in vivo and in vitro, which evidenced the inhibition of gastric cancer EMT viaregulating the NF-κB inflammatory pathway.

目的:研究放线菌多糖(ACPS)对胃癌细胞侵袭和转移的影响机制:研究放线菌多糖(ACPS)对胃癌细胞侵袭和转移的影响机制:方法:用稳定转染荧光素酶基因的BGC-823-Luc胃癌细胞建立体内移植肿瘤小鼠模型。活体小鼠成像系统用于观察肿瘤生长,苏木精和伊红染色用于分析组织病理学。透孔试验和划痕伤口试验用于检测 BGC-823 细胞的侵袭和迁移能力。免疫荧光、共聚焦显微镜、免疫组织化学和 Western 印迹分析用于分析核转录因子-κB(NF-κB)信号通路和上皮-间质转化(EMT)相关蛋白的表达:结果:ACPS能明显抑制裸鼠皮下移植的BGC-823-Luc胃癌肿瘤的生长,并减少肿瘤组织中的炎症细胞浸润。ACPS 可抑制表皮生长因子诱导的 BGC-823 细胞的侵袭、迁移和细胞骨架的形态变化。ACPS 可抑制胃癌的 EMT,降低移植肿瘤组织中基质金属肽酶 9、N-cadherin 和 p-NF-κB p65 的表达。ACPS 可抑制 BGC-823 细胞中基质金属蛋白酶和血管粘附因子的表达,促进 p65-NF-κB 核转位,并调节与 NF-κB p65 通路相关的蛋白:结论:ACPS可抑制胃癌的体内和体外侵袭和转移,证明其可通过调节NF-κB炎症通路抑制胃癌的EMT。
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引用次数: 0
Weitiao No. 3 (3) enhances the efficacy of anti-programmed cell death protein-1 immunotherapy by modulating the intestinal microbiota in an orthotopic model of gastric cancer mice. 潍胶 3 号(3)通过调节胃癌小鼠正位模型中的肠道微生物群,提高了抗程序性细胞死亡蛋白-1 免疫疗法的疗效。
Pub Date : 2024-10-01 DOI: 10.19852/j.cnki.jtcm.2024.05.002
Huang Xiaona, L I Yuzhen, Zhu Chenyang, Zhu Hengzhou, Jiang Chenyu, Zhu Xiaodan, Zhang Chencen, Jin Chunhui

Objective: To explore the effects of Weitiao No. 3 (3, WD-3) on anti-programmed cell death protein-1 (PD-1) immunotherapy in gastric cancer (GC).

Methods: The intestinal microbiota was analyzed by 16S rDNA sequencing of fecal samples from three groups: healthy people (Health), GC patients (GC), and WD-3-treated GC patients (WD-3). Next, we established an orthotopic model of GC mice, which were treated with anti-PD-1, WD-3, or an inoculation of intestinal bacteria. Immune markers CD3, CD4, CD8, and forkhead box protein P3 (FOXP3), and the cell proliferation marker Ki67, were evaluated by immunohistochemistry. Cell apoptosis in GC tumors was assessed by terminal-deoxynucleotidyl-transferase-mediated deoxyuridine triphosphate nick end labeling staining. Enzyme-linked immunosorbent assays (ELISAs) were performed to analyze the serum levels of the following cytokines in GC mice: tumor necrosis factor (TNF)-α, interleukin (IL)-2, IL-6, IL-10, interferon (IFN)-γ, and transforming growth factor (TGF)-β.

Results: Sequencing data showed that there were significant differences in the composition of the gut microbial community among the three human groups. The gut bacteria in the three groups mainly comprised the phyla Firmicutes, Proteobacteria, Bacteroidetes, and Actinobacteria. At the genus level, the relative abundances of Bifidobacterium and Coprococcus showed significant decreases in the GC group, and an obvious increase in the WD-3 group, compared with the Health group. Interestingly, the relative abundance of Saccharopolyspora was only detected in the WD-3 group. The results of in vivo experiments in GC mice showed that WD-3 or anti-PD-1 treatment increased the levels of CD3+, CD4+, and CD8+ T cells, but decreased the levels of FOXP3+ regulatory T cells. Furthermore, WD-3 or PD-1 antibody treatment inhibited proliferation and promoted apoptosis of GC tumor cells. ELISA analysis showed that WD-3 or PD-1 antibody treatment facilitated TNF-α, IL-2, and IFN-γ expression, while suppressing IL-6, IL-10, and TGF-β expression. Combination therapy with WD-3 and anti-PD-1 intensified all of these effects.

Conclusion: WD-3 enhanced the immunotherapeutic efficacy of anti-PD-1 by modulating the intestinal microbiota in an orthotopic model of GC mice.

目的方法:通过对健康人(Health)、胃癌患者(GC)和WD-3治疗组的粪便样本进行16S rDNA测序,分析肠道微生物区系:方法:通过对健康人(Health)、胃癌患者(GC)和WD-3治疗的胃癌患者(WD-3)三组粪便样本进行16S rDNA测序,分析肠道微生物群。接着,我们建立了一个 GC 小鼠正位模型,用抗 PD-1、WD-3 或肠道细菌接种治疗这些小鼠。免疫组化法评估了免疫标记物 CD3、CD4、CD8、叉头盒蛋白 P3(FOXP3)和细胞增殖标记物 Ki67。GC肿瘤的细胞凋亡通过末端脱氧核苷酸转移酶介导的脱氧尿苷三磷酸缺口末端标记染色进行评估。酶联免疫吸附试验(ELISA)分析了 GC 小鼠血清中下列细胞因子的水平:肿瘤坏死因子(TNF)-α、白细胞介素(IL)-2、IL-6、IL-10、干扰素(IFN)-γ 和转化生长因子(TGF)-β:测序数据显示,三组人的肠道微生物群落组成存在显著差异。三组人的肠道细菌主要包括固着菌门、变形菌门、类杆菌门和放线菌门。在菌属水平上,与健康组相比,双歧杆菌和铜绿菌的相对丰度在 GC 组显著下降,而在 WD-3 组则明显上升。有趣的是,只有在 WD-3 组中检测到了糖孢子菌的相对丰度。GC 小鼠体内实验结果显示,WD-3 或抗 PD-1 治疗可增加 CD3+、CD4+ 和 CD8+ T 细胞的水平,但会降低 FOXP3+ 调节性 T 细胞的水平。此外,WD-3 或 PD-1 抗体治疗可抑制 GC 肿瘤细胞的增殖并促进其凋亡。ELISA分析表明,WD-3或PD-1抗体治疗可促进TNF-α、IL-2和IFN-γ的表达,同时抑制IL-6、IL-10和TGF-β的表达。WD-3和抗PD-1的联合治疗加强了所有这些效果:结论:WD-3通过调节肠道微生物群增强了抗PD-1在GC小鼠正位模型中的免疫治疗效果。
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引用次数: 0
Assessment of phytochemicals, antioxidant, anti-hemolytic, anti-inflammatory and anti-cancer potential of flowers, leaves and stem extracts of. 评估花、叶和茎提取物的植物化学成分、抗氧化、抗溶血、抗炎和抗癌潜力。
Pub Date : 2024-08-01 DOI: 10.19852/j.cnki.jtcm.2024.04.001
Zubaria Tul Ain, Iram Fatima, Sana Naseer, Sobia Kanwal, Tariq Mahmood

Objective: To evaluate phytochemicals and in vitro biological potential of flowers, leaves and stem extracts of Rosa arvensis.

Methods: Presence of twenty secondary metabolites was confirmed and then phenolic and flavonoid contents were quantified spectrophotometrically. Fourier Transform Infrared spectroscopy was conducted to ascertain functional groups and antioxidant potential was examined using 2,2-diphenyl-1-picrylhydrazyl scavenging activity, total antioxidant capacity and total reducing power assays. Human erythrocytes were used to assess anti-hemolytic activity and five bacterial strains were examined to determine antibacterial potential of plant extracts. Radish seeds were used to perform phytotoxic activity and cytotoxic potential was evaluated via brine shrimps and PC3 cell lines.

Results: Highest phenolic contents were detected in the methanolic extract of Rosa arvensis flower (RAFM) [(151.635 ± 0.005) gallic acid equivalent mg/g] and highest flavonoid contents in the chloroform leaf extract (RALC) [(108.228 ± 0.004) quercetin equivalent mg/g]. Fourier-transform infrared spectroscopy analysis showed the presence of wide range of functional groups. The antioxidant assays indicated highest DPPH scavenging activity [IC50 (23.5 ± 0.6) μg/mL] in the methanolic stem extract (RASM), highest total antioxidant capacity [(265.1 ± 0.9) μg/mL] in RAFM and highest reducing potential [(209.9 ± 0.6) μg/mL] in leaf extract (RALM). Highest anti-hemolytic activity [(90.0 ± 0.5) μg/mL] was recorded in RAFM and brine shrimp cytotoxicity potential [(52.3 ± 0.3) μg/mL] in RASM. The antimicrobial activity was detected highest [(21.1 ± 0.5) mm inhibition zones] in RALM against Streptococcus aureus. In the end, anti-inflammatory and anti-cancer activity results depicted less than 50 % inhibition in the methanolic extracts. CONCLUSIONS: Our findings will be helpful in designing pharmaceutical regimens and therefore, more studies can be recommended to isolate and characterize compounds associated with the biological activities of Rosa arvensis.

目的:评估蔷薇花、叶和茎提取物的植物化学成分和体外生物学潜力:评估蔷薇花、叶和茎提取物的植物化学成分和体外生物学潜力:方法:确认了二十种次级代谢产物的存在,然后用分光光度法对酚类和类黄酮的含量进行了定量。采用傅立叶变换红外光谱法确定功能基团,并利用 2,2-二苯基-1-苦基肼清除活性、总抗氧化能力和总还原力检测抗氧化潜力。利用人体红细胞评估抗溶血活性,并检测五种细菌菌株,以确定植物提取物的抗菌潜力。萝卜种子被用来进行植物毒性试验,盐水虾和 PC3 细胞系被用来评估细胞毒性潜力:结果:蔷薇花甲醇提取物(RAFM)中酚含量最高[(151.635 ± 0.005)没食子酸当量毫克/克],氯仿叶提取物(RALC)中黄酮含量最高[(108.228 ± 0.004)槲皮素当量毫克/克]。傅立叶变换红外光谱分析显示了多种官能团的存在。抗氧化试验表明,甲醇茎提取物(RASM)的 DPPH 清除活性最高[IC50 (23.5 ± 0.6) μg/mL],RAFM 的总抗氧化能力最高[(265.1 ± 0.9) μg/mL],叶提取物(RALM)的还原电位最高[(209.9 ± 0.6) μg/mL]。在 RAFM 中记录到最高的抗溶血活性[(90.0 ± 0.5)μg/mL],在 RASM 中记录到最高的盐水虾细胞毒性潜能[(52.3 ± 0.3)μg/mL]。RALM 对金黄色葡萄球菌的抗菌活性最高[(21.1 ± 0.5)毫米抑菌区]。最后,甲醇提取物的抗炎和抗癌活性抑制率低于 50%。结论:我们的研究结果将有助于设计药物治疗方案,因此建议开展更多研究,以分离和鉴定与蔷薇生物活性相关的化合物。
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引用次数: 0
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. 通窍益智颗粒抑制海马核因子卡巴-b/核苷酸寡聚化结构域样受体3/caspase-1热解通路,对抗大鼠血管性痴呆。
Pub Date : 2024-08-01 DOI: 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.

目的在大鼠模型中探讨通窍益智颗粒(TQYZKL)干预血管性痴呆(VaD)的机制:方法:通过双血管闭塞(2VO)建立大鼠血管性痴呆模型。大鼠随机分为 Sham 组、模型组、尼莫地平组、TQYZKL(6.2 g?kg-1?d-1)组、TQYZKL(12.4 g?kg-1?d-1)组、TQYZKL(24.8 g?kg-1?d-1)组。进行Morris水迷宫(MWM)测试以检测学习和记忆功能;血栓素-伊红染色和透射电子显微镜(TEM)观察海马的病理损伤;Tunel荧光染色检测海马神经元的脓毒症。利用Western印迹和反转录聚合酶链反应检测了与热蛋白沉积相关的蛋白,即高尔基外周膜蛋白p65(P65)、核苷酸寡聚化结构域样受体3(NLRP3)、caspase-1和Gasdermin D(GSDMD)的表达水平。此外,还通过酶联免疫吸附试验测定了血清中白细胞介素-1β(IL-1β)和白细胞介素-18(IL-18)的水平:研究发现,TQYZKL能有效提高VaD大鼠的学习和记忆能力,缓解海马的病理损伤,恢复神经元形态,降低热蛋白相关蛋白P65、NLRP3、caspase-1、GSDMD-N、IL-18和IL-1β的表达(P<0.05):TQYZKL通过调节核因子卡巴-B/NLRP3/caspase-1信号通路,抑制VaD大鼠海马神经元的脓毒症,从而对VaD大鼠产生治疗作用。
{"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":"44 4","pages":"680-687"},"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}
引用次数: 0
Effect of Jiedu Huayu decoction on oral mucosal Axin and β-catenin expression in oral submucosal fibrosis model rats. 解毒化瘀汤对口腔黏膜下纤维化模型大鼠口腔黏膜Axin和β-catenin表达的影响
Pub Date : 2024-08-01 DOI: 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.

目的研究中药方剂解毒化瘀汤对口腔黏膜下纤维化(OSF)大鼠口腔黏膜的保护作用及其潜在作用机制:方法:通过注射甜菜碱和局部涂抹建立Sprague-Dawley雄性OSF模型大鼠,随机分组,灌胃给药4周。在用药前后测量张口和颊粘膜评分白细胞介素水平、Axin和β-catenin蛋白或基因的表达:结果:用JHD治疗后,大鼠口腔黏膜病变明显减轻,Axin蛋白和mRNA表达明显增加,β-catenin蛋白和mRNA表达明显减少,白细胞介素-1β和白细胞介素-6水平降低,白细胞介素-10水平升高:JHD能有效缓解OSF大鼠口腔黏膜的病理损伤,其作用机制可能与促进Axin表达和抑制β-catenin表达有关。
{"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":"44 4","pages":"688-693"},"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}
引用次数: 0
Spore Oil enhances the effect of cyclophosphamide inhibiting programmed death-1 and prolongs the survival of H22 tumor-bearing mice. 孢子油能增强环磷酰胺抑制程序性死亡-1的效果,延长H22肿瘤小鼠的存活时间。
Pub Date : 2024-08-01 DOI: 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.

研究目的研究灵芝孢子油(GLSO)对环磷酰胺(CTX)治疗H22肿瘤小鼠肿瘤生长和生存的影响,并探讨其潜在机制:方法:应用异种移植H22肝细胞癌小鼠模型研究GLSO对肿瘤生长和动物生存的影响,并采用Kaplan-Meier生存分析法分析动物的生存期。血浆生化检查用于检测丙氨酸氨基转移酶(ALT)、天冬氨酸氨基转移酶(AST)、尿素(UREA)和肌酐(CRE)的水平。对程序性死亡-1(PD-1)、程序性死亡配体1(PD-L1)、Janus激酶2(JAK2)、磷酸化信号转导和转录激活因子3(p-STAT3)以及信号转导和转录激活因子3(STAT3)的表达进行了蛋白质印迹分析:结果:GLSO提高了CTX的抗肿瘤效果,延长了接受CTX治疗的H22肿瘤小鼠的生存期。同时,GLSO能提高胸腺指数,对动物肝功能无明显毒性。GLSO 还能降低接受 CTX 治疗的 H22 肿瘤小鼠体内的脲尿酸水平。此外,GLSO还能抑制脾脏中PD-1的表达,这与JAK2的表达和STAT3的磷酸化无关。然而,GLSO并不影响肿瘤组织中PD-L1、JAK2和p-STAT3的表达:结论:GLSO 可增强 CTX 的抗肿瘤作用,延长 H22 肿瘤小鼠的寿命,其潜在机制可能与胸腺功能的改善作用和抑制 PD-1 在脾脏的表达有关。此外,这些研究结果还表明,在肝细胞癌的临床化疗中,GLSO与CTX联用可延长患者的生存期。
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引用次数: 0
Zhuangyao Jianshen pill ameliorates testosterone-induced benign postatic hyperplasia in rats. 壮腰健腰丸可改善睾酮诱导的大鼠良性肝后增生。
Pub Date : 2024-08-01 DOI: 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.

目的确定壮阳健脾丸(ZYJSP)对良性前列腺增生症(BPH)的治疗作用,并探讨其潜在机制:方法:将48只雄性Sprague-Dawley大鼠随机分为6组:对照组、良性前列腺增生模型组、非那雄胺处理组、ZYJSP低、中、高剂量组。除对照组外,其余 40 只大鼠均被阉割,并连续 28 天注射丙酸睾酮(TP)诱导良性前列腺增生。同时灌胃相应的药物。测定前列腺湿重、前列腺指数(PI)和前列腺组织病理学变化,作为研究 ZYJSP 对良性前列腺增生症疗效的依据。测定血清性激素水平、氧化应激标志物、炎症标志物、肾功能标志物、生长因子和前列腺中 Cyclin D1 的表达,以确定 ZYJSP 对良性前列腺增生症的治疗机制:结果:服用 ZYJSP 能明显减轻 TP 治疗的阉割大鼠的前列腺湿重和 PI,并改善前列腺的组织学变化。TP明显增加了血清中肌酐、血尿素氮和生长因子的水平,也增加了前列腺中细胞周期蛋白D1的表达。ZYJSP 能显著降低这些指标中的大部分。ZYJSP 能明显恢复 TP 引起的睾酮、雌二醇和双氢睾酮的失调。此外,ZYJSP 还能缓解 TP 引起的前列腺损伤,并通过降低白细胞介素-6、白细胞介素-8 和丙二醛水平以及提高血清中超氧化物歧化酶的活性,表现出抗炎和抗氧化活性:这些研究结果表明,ZYJSP能有效改善阉割大鼠由TP诱导的良性前列腺增生症,其潜在机制可能与调节性激素平衡、减少氧化应激和抑制炎症反应有关。
{"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":"44 4","pages":"694-702"},"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}
引用次数: 0
Luteolin promotes neuronogenesis in hippocampus of chronic unpredictable mild stress rats and primary hippocampus of fetal rats. 叶黄素能促进慢性不可预知轻度应激大鼠海马和胎鼠初级海马的神经元生成。
Pub Date : 2024-08-01 DOI: 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":"44 4","pages":"670-679"},"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}
引用次数: 0
Adenosine triphosphate mediates the pain tolerance effect of manual acupuncture at Zusanli (ST36) in mice. 三磷酸腺苷介导小鼠手针灸足三里(ST36)的疼痛耐受效应。
Pub Date : 2024-08-01 DOI: 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":"44 4","pages":"660-669"},"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}
引用次数: 0
Study on the anti-inflammatory mechanism of moxibustion in rheumatoid arthritis in rats based on phospholipaseA2 signaling inhibition by Annexin 1. 基于Annexin 1抑制磷脂酶A2信号传导的艾灸对大鼠类风湿性关节炎抗炎机制的研究
Pub Date : 2024-08-01 DOI: 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.

目的方法:将30只雄性Sprague-Dawley大鼠随机分为5组(每组6只),分别为空白对照组(CON)、类风湿性关节炎模型组(RA)、艾灸组(RA):将30只雄性Sprague-Dawley大鼠随机分为5组(每组6只):空白对照(CON)组、RA模型(RA)组、艾灸(MOX)组、Annexin 1慢病毒干预(RNAi-Anxa1)组和Annexin 1慢病毒干预+艾灸(RNAi-Anxa1 + MOX)组。RNAi-Anxa1组和RNAi-Anxa1 + MOX组大鼠的足垫注射了慢病毒载体介导的RNAi-Anxa1。通过向RA组、MOX组、RNAi-Anxa1组和RNAi-Anxa1 + MOX组注射弗氏完全佐剂(FCA),建立了实验性RA大鼠模型。MOX 组和 RNAi-Anxa1 + MOX 组的大鼠接受艾灸治疗。建模后,用艾条灸 "神枢(BL23)"和 "足三里(ST36)",每穴均灸5次,双侧交替进行,每天1次,6次为1个疗程,疗程间休息1天。共进行三个疗程。在实验第 1、7、14、21 和 28 天,使用游标卡尺测量双侧衬垫厚度。用 Western 印迹法观察病变关节滑膜中 cPLA2α 信号的表达。用苏木精-伊红(HE)染色法观察大鼠踝关节滑膜的病理变化。用酶联免疫吸附法检测白细胞介素(IL)-1β、IL-10、前列腺素 E2(PGE2)和白三烯 B4(LTB4):结果:艾灸提高了 Annexin 1 的水平,减轻了 RA 大鼠的炎症反应。结果:艾灸增加了 Annexin 1 的表达,抑制了 cPLA2α 的磷酸化表达,降低了血清中 IL-1β、PGE2 和 LTB4 的水平,增加了 IL-10 的水平。艾灸干预Annexin 1慢病毒后的RA大鼠血清中IL-1β、PGE2、LTB4和IL-10水平几乎没有变化:结论:艾灸增强了对cPLA2α信号通路的负调控,增加了滑膜Annexin 1的表达,抑制了cPLA2α信号通路,间接抑制了下游炎症因子的表达,起到了减轻炎症的作用。
{"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":"44 4","pages":"753-761"},"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}
引用次数: 0
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Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan
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