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Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan最新文献

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International standard of Traditional Chinese Medicine techniques: the operating specification for Traditional Chinese Medicine enema (2022). 中医药技术国际标准:中药灌肠操作规范(2022 年)。
Pub Date : 2024-10-01 DOI: 10.19852/j.cnki.jtcm.2024.05.010
Y U Miao, Pei Xiaohua

Chinese Medicine Enema is one of the external therapies in Traditional Chinese Medicine (TCM), which has been widely used clinically. The "International Standard of Traditional Chinese Medicine Techniques: The Operating Specifications for Chinese Medicine Enema is drawn up by the Beijing Hospital of Traditional Chinese Medicine affiliated to Capital Medical University and Beijing University of Chinese Medicine Xiamen Hospital in collaboration with domestic TCM universities and hospitals. The specification includes definition, operating process, points for attention and contraindications. It is targeted to provide reference for TCM providers at home and abroad with TCM background in clinical decision-making.

中药灌肠是中医外治法之一,在临床上应用广泛。中药灌肠操作规范》由首都医科大学附属北京中医医院制定:中药灌肠操作规范》由首都医科大学附属北京中医医院、北京中医药大学附属厦门医院联合国内中医药大学和医院共同制定。规范内容包括定义、操作流程、注意事项和禁忌症。旨在为国内外具有中医背景的中医医疗机构提供临床决策参考。
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引用次数: 0
Regulatory effects of the p38 mitogen-activated protein kinase-myosin light chain kinase pathway on the intestinal epithelial mechanical barrier and the mechanism of modified Pulsatilla decoction in the treatment of ulcerative colitis. p38丝裂原活化蛋白激酶-肌球蛋白轻链激酶通路对肠上皮细胞机械屏障的调节作用以及改良白头翁煎剂治疗溃疡性结肠炎的机制。
Pub Date : 2024-10-01 DOI: 10.19852/j.cnki.jtcm.20240806.006
W U Tingting, Yang Xin, Zhu Huiping, Guo Jinwei, Zhu Hui, Zhang Peipei, Wang Meng, Liang Guoqiang, Sun Hongwen

Objective: To investigate the mechanism of the protective effect of modified Pulsatilla decoction (, MPD) on the mechanical barrier of the ulcerative colitis (UC) intestinal epithelium in vitro and in vivo.

Methods: We established an intestinal epithelial crypt cell line-6 cell barrier injury model by using lipopolysaccharide (LPS). The model was then treated with p38 mitogen-activated protein kinase-myosin light chain kinase (p38MAPK-MLCK) pathway inhibitors, p38MAPK-MLCK pathway silencing genes (si-p38MAPK, si-NF-κB, and si-MLCK), and MPD respectively. Transepithelial electronic resistance (TEER) measurements and permeability assays were performed to assess barrier function. Immunofluorescence staining of tight junctions (TJ) was performed. In in vivo experiment, dextran sodium sulfate-induced colitis rat model was conducted to evaluate the effect of MPD and mesalazine on UC. The rats were scored using the disease activity index based on their clinical symptoms. Transmission electron microscopy and hematoxylin-eosin staining were used to examine morphological changes in UC rats. Western blotting and real-time quantitative polymerase chain reaction were performed to examine the gene and protein expression of significant differential molecules.

Results: In in vitro study, LPS-induced intestinal barrier dysfunction was inhibited by p38MAPK-MLCK pathway inhibitors and p38MAPK-MLCK pathway gene silencing. Silencing of p38MAPK-MLCK pathway genes decreased TJ expression. MPD treatment partly restored the LPS-induced decreased in TEER and increase in permeability. MPD increased the gene and protein expression of TJ, while down-regulated the LPS-induced high expression of p-p38MAPK and p-MLC. In UC model rats, MPD could ameliorate body weight loss and disease activity index, relieve colonic pathology, up-regulate TJ expression as well as decrease the expression of p-p38MAPK and p-MLC in UC rat colonic mucosal tissue.

Conclusions: The p38MAPK-MLCK signaling pathway can affect mechanical barrier function and TJ expression in the intestinal epithelium. MPD restores TJ expression and attenuates intestinal epithelial barrier damage by suppressing the p38MAPK-MLCK pathway.

目的研究改良白头翁煎剂(MPD)在体外和体内对溃疡性结肠炎(UC)肠上皮细胞机械屏障保护作用的机制:方法:我们利用脂多糖(LPS)建立了肠上皮隐窝细胞系-6细胞屏障损伤模型。然后分别用 p38 丝裂原活化蛋白激酶-肌球蛋白轻链激酶(p38MAPK-MLCK)通路抑制剂、p38MAPK-MLCK 通路沉默基因(si-p38MAPK、si-NF-κB 和 si-MLCK)和 MPD 处理该模型。进行跨上皮电子阻力(TEER)测量和渗透性试验以评估屏障功能。对紧密连接(TJ)进行免疫荧光染色。在体内实验中,进行了葡聚糖硫酸钠诱导的大鼠结肠炎模型,以评估 MPD 和美沙拉嗪对 UC 的影响。根据大鼠的临床症状,采用疾病活动指数对其进行评分。透射电子显微镜和苏木精-伊红染色用于观察 UC 大鼠的形态学变化。Western 印迹和实时定量聚合酶链反应用于检测重要差异分子的基因和蛋白表达:结果:在体外研究中,p38MAPK-MLCK 通路抑制剂和 p38MAPK-MLCK 通路基因沉默抑制了 LPS 诱导的肠屏障功能障碍。p38MAPK-MLCK通路基因沉默会降低TJ的表达。MPD 处理可部分恢复 LPS 诱导的 TEER 减少和渗透性增加。MPD 增加了 TJ 的基因和蛋白表达,同时下调了 LPS 诱导的 p-p38MAPK 和 p-MLC 的高表达。在 UC 模型大鼠中,MPD 可改善体重下降和疾病活动指数,缓解结肠病理变化,上调 TJ 的表达,并降低 UC 大鼠结肠粘膜组织中 p-p38MAPK 和 p-MLC 的表达:结论:p38MAPK-MLCK 信号通路可影响肠上皮细胞的机械屏障功能和 TJ 表达。MPD可通过抑制p38MAPK-MLCK通路恢复TJ表达,减轻肠上皮屏障损伤。
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引用次数: 0
A pilot study of precision treatment for patients with lung cancer pain by Longteng Tongluo recipe using serum genomics. 龙腾通络方利用血清基因组学对肺癌疼痛患者进行精准治疗的试点研究。
Pub Date : 2024-10-01 DOI: 10.19852/j.cnki.jtcm.20240828.005
W U Ruixin, Fang Qingliang, Guan Sisi, Wei Xianglong, Shan Mengjun, Mao Zhujun, Gong Yabin, X U Ling, Zhou Di, Dong Changsheng
<p><strong>Objective: </strong>To investigate the efficacy of Longteng Tongluo recipe (, LTTL) combined with three-step analgesia for the treatment of lung cancer pain, and the changes in serum miRNA expressions before- and after treatment with LTTL and its correlation with lung cancer pain. The possible mechanism underlying LTTL effects on the treatment of lung cancer pain was conducted.</p><p><strong>Methods: </strong>The pilot study was conducted at the oncology ward of the Yueyang Hospital and the Longhua Hospital between March 2018 and October 2019. A prospective, single-blind, placebo controlled, randomized clinical trial of LTTL or placebo combined with three-step analgesia treatments were administered to 24 cancer pain patients diagnosed with lung cancer. Analgesic efficacy was investigated as the primary outcome. Equivalent morphine consumption and numerical rating scale (NRS) scores were used as the secondary outcome. In the present study, we utilized deep sequencing techniques to compare the differential miRNA expressions in serum samples obtained from two groups: the lung cancer pain treatment group (LTTL + three-step analgesia) and the control group (placebo + three-step analgesia). Next, we employed the target prediction database to investigate the target genes for differential miRNA expressions and Gene Ontology (GO) analysis along with Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis to examine the roles and the major biochemical and signaling pathways related to the differentially expressed target genes, respectively.</p><p><strong>Results: </strong>LTTL treatment significantly reduces the NRS score (<i>P =</i> 0.021) as compared to those before treatment, along with significant reductions in the total morphine equivalent consumption (<i>P =</i> 0.007) and the average daily equivalent morphine consumption (<i>P =</i> 0.003) as opposed to the control group. The expressions of 31 miRNAs differed considerably between the two groups of patients (≥ 2 times up-modulated or down-regulated between these groups, <i>P</i><0.05). For instance, the miRNAs expression levels for patients before treatment (has-miR-2110 and has-miR-7d-3p) were significantly enhanced as compared to the healthy people, after LTTL treatment, the expressions of miR-2110 and miR-7d-3p in patients with lung cancer pain reduced significantly. Studies show that the above two miRNAs were significantly associated with lung cancer pain, which could mediate lung cancer pain. Furthermore, we identified 355 genes as potential targets of the 31 differentially expressed miRNAs. Pathway enrichment analyses using KEGG and GO analysis indicated that these target genes may play a crucial role in the development and modulation of lung cancer pain.</p><p><strong>Conclusion: </strong>LTTL demonstrated a discernible impact on alleviating lung cancer pain and its mechanism of action may be related to the downregulation of has-miR-2110 and has-miR-7d-3p expressi
研究目的探讨龙藤通络汤联合三阶梯镇痛治疗肺癌疼痛的疗效,以及龙藤通络汤治疗前后血清miRNA表达的变化及其与肺癌疼痛的相关性。研究还探讨了LTL治疗肺癌疼痛的可能机制:试验研究于2018年3月至2019年10月期间在岳阳医院和龙华医院肿瘤科病房进行。对24例确诊为肺癌的癌痛患者进行LTL或安慰剂联合三阶梯镇痛治疗的前瞻性、单盲、安慰剂对照、随机临床试验。镇痛效果是主要研究结果。等效吗啡消耗量和数字评分量表(NRS)评分作为次要结果。在本研究中,我们利用深度测序技术比较了肺癌疼痛治疗组(LTL + 三步镇痛法)和对照组(安慰剂 + 三步镇痛法)两组血清样本中不同的 miRNA 表达。接下来,我们利用靶标预测数据库研究了 miRNA 差异表达的靶基因,并利用基因本体(GO)分析和京都基因组百科全书(KEGG)通路富集分析分别研究了与差异表达靶基因相关的作用和主要生化及信号通路:结果:与治疗前相比,LTL治疗可明显降低NRS评分(P = 0.021),与对照组相比,总吗啡当量消耗量(P = 0.007)和平均每日吗啡当量消耗量(P = 0.003)也明显降低。两组患者中 31 种 miRNA 的表达差异很大(上调或下调≥ 2 倍):LTL对减轻肺癌疼痛有明显作用,其作用机制可能与下调has-miR-2110和has-miR-7d-3p的表达有关。这项试验研究为进一步探索 LTTL 在肺癌疼痛患者中的应用提供了支持。
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引用次数: 0
Clinical value of modified Shenling Baizhu powder in treating targeted therapy-induced diarrhea in non-small cell lung cancer. 改良神灵白术散治疗非小细胞肺癌靶向治疗引起的腹泻的临床价值
Pub Date : 2024-10-01 DOI: 10.19852/j.cnki.jtcm.20240806.008
Wang Ming, Zheng Yun

Objective: To assess clinical value of modified Shenling Baizhu powder (, SBP) in intervening targeted therapy-induced diarrhea.

Methods: This study was a prospective randomized controlled study. Eighty-five non-small cell lung cancer (NSCLC) patients with diarrhea who took targeted drugs were randomly divided into two groups. The experimental group received modified SBP, while the control group received imodium. During 2 courses of treatment (1 week/course) and 2 weeks of follow-up, we observed remission and recurrence of diarrhea, as well as the improvement of Karnofsky score (KPS) in the two groups and drug safety.

Results: Eighty cases were completed, with 40 cases in the experimental group and 40 cases in the control group. The control group's diarrhea remission rate was significantly lower than the experimental group's (P<0.05). After 2 courses of treatment, the symptom scores of both groups were lower than before, with that of the experimental group remarkably lower (P<0.05). Furthermore, the experimental group experienced less abdominal fullness and appetite loss than the control group (P<0.05). There was no prominent difference in overall diarrhea recurrence, time, or KPS after treatment between the two groups (P>0.05). No unique adverse events occurred in experimental group or control group.

Conclusion: The modified SBP could improve targeted therapy-induced diarrhea in NSCLC, and is superior to imodium in relieving diarrhea, improving related symptom scores and symptoms, with no obvious drug-related adverse events.

目的评估改良神灵白术粉(SBP)在干预靶向治疗引起的腹泻中的临床价值:本研究为前瞻性随机对照研究。85 名服用靶向药物的非小细胞肺癌(NSCLC)腹泻患者被随机分为两组。实验组服用改良 SBP,对照组服用易蒙停。在2个疗程(1周/疗程)和2周的随访中,我们观察了两组患者腹泻的缓解和复发情况,以及Karnofsky评分(KPS)的改善情况和用药安全性:共完成 80 例治疗,其中实验组 40 例,对照组 40 例。对照组腹泻缓解率明显低于实验组(PPPP>0.05)。实验组和对照组均未发生特殊不良反应:改良SBP可改善靶向治疗诱发的NSCLC腹泻,在缓解腹泻、改善相关症状评分和症状方面优于易蒙停,且无明显药物相关不良反应。
{"title":"Clinical value of modified Shenling Baizhu powder in treating targeted therapy-induced diarrhea in non-small cell lung cancer.","authors":"Wang Ming, Zheng Yun","doi":"10.19852/j.cnki.jtcm.20240806.008","DOIUrl":"10.19852/j.cnki.jtcm.20240806.008","url":null,"abstract":"<p><strong>Objective: </strong>To assess clinical value of modified Shenling Baizhu powder (, SBP) in intervening targeted therapy-induced diarrhea.</p><p><strong>Methods: </strong>This study was a prospective randomized controlled study. Eighty-five non-small cell lung cancer (NSCLC) patients with diarrhea who took targeted drugs were randomly divided into two groups. The experimental group received modified SBP, while the control group received imodium. During 2 courses of treatment (1 week/course) and 2 weeks of follow-up, we observed remission and recurrence of diarrhea, as well as the improvement of Karnofsky score (KPS) in the two groups and drug safety.</p><p><strong>Results: </strong>Eighty cases were completed, with 40 cases in the experimental group and 40 cases in the control group. The control group's diarrhea remission rate was significantly lower than the experimental group's (<i>P</i><0.05). After 2 courses of treatment, the symptom scores of both groups were lower than before, with that of the experimental group remarkably lower (<i>P</i><0.05). Furthermore, the experimental group experienced less abdominal fullness and appetite loss than the control group (<i>P</i><0.05). There was no prominent difference in overall diarrhea recurrence, time, or KPS after treatment between the two groups (<i>P</i>>0.05). No unique adverse events occurred in experimental group or control group.</p><p><strong>Conclusion: </strong>The modified SBP could improve targeted therapy-induced diarrhea in NSCLC, and is superior to imodium in relieving diarrhea, improving related symptom scores and symptoms, with no obvious drug-related adverse events.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":"44 5","pages":"1000-1005"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11462525/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142396425","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 phosphatase and tensin homolog-induced putative kinase 1/ E3 ubiquitin ligase Parkin mediated mitochondrial autophagy on chronic kidney disease myocardial injury and the intervention mechanism of Shenshuai recipe. 磷酸酶和天丝同源物诱导的推定激酶1/E3泛素连接酶Parkin介导的线粒体自噬对慢性肾脏病心肌损伤的影响及神水方的干预机制
Pub Date : 2024-10-01 DOI: 10.19852/j.cnki.jtcm.20231231.001
Zhang Gedi, Liu Gengxin, Guo Min, Luo Fuli, Yan Ziyou, G E Wei

Objective: To study whether Shenshuai recipe (, SSR) can play a protective role on chronic kidney disease myocardial injury model through phosphatase and tensin homolog-induced putative kinase 1 (PINK1)/E3 ubiquitin ligase Parkin (Parkin) mitochondrial autophagy pathway.

Methods: Forty-eight nephrectomized rats were randomly divided into six groups: sham-operated group, model group, Benazepril group, low, medium and high-dose groups of SSR. The rats were given the cor-responding intervention for six weeks, then were sacrificed. Serum was examined by enzyme linked immunosorbent assay (ELISA). Cardiac ultrasound was used to detect cardiac function in 5/6 nephrectomized rats. Myocardial tissue was examined by light and electron microscopy; PINK1, Parkin, microtubule-associated protein1 light chain 3 II (LC3B), sequestosome 1 (P62), BECN1 (Beclin-1) and dynamin-related protein 1 (Drp-1) were measured by real time polymerase chain reaction (RT-PCR), Western blot (WB) and immunohistochemistry (IHC).

Results: The expression levels of blood urea nitrogen (BUN) and creatinine (SCr) in the model group were significantly higher than those in the sham-operated group, indicating that modeling was successful. SSR can protect myocardium by reducing the relative expression of creatine kinase myocardial isoenzyme and hypersensitivity cardiac troponin I (P<0.05). SSR can improve cardiac function in rats after ultrasound testing. SSR can improve the pathological manifestations of myocardial tissue after Masson staining. SSR can increase the number of autophagosomes and autophagiclysosomes in 5/6 nephrectomized rats (P<0.05). Determined by RT-PCR, WB and IHC, SSR can increase the relative expression of PINK1, Parkin, and LC3B (P<0.05), and decrease the relative expression of P62, Beclin-1 and Drp-1 (P<0.05).

Conclusions: The PINK1/Parkin mitochondrial autophagy pathway in myocardial tissues in 5/6 nephrectomy CKD myocardial injury rats was inhibited. SSR can activate PINK1/Parkin mitochondrial autophagy to enhance mitochondrial autophagy, and play a protective role in myocardial tissues.

研究目的研究神水方(SSR)能否通过磷酸酶和天丝同源物诱导的假定激酶1(PINK1)/E3泛素连接酶Parkin(Parkin)线粒体自噬途径对慢性肾脏病心肌损伤模型起到保护作用:将 48 只肾切除大鼠随机分为 6 组:假手术组、模型组、贝那普利组、低、中、高剂量 SSR 组。大鼠接受相应干预六周后处死。用酶联免疫吸附试验(ELISA)检测血清。用心脏超声检测 5/6 肾切除大鼠的心脏功能。通过实时聚合酶链反应(RT-PCR)、免疫印迹(WB)和免疫组织化学(IHC)检测 PINK1、Parkin、微管相关蛋白 1 轻链 3 II(LC3B)、序列组 1(P62)、BECN1(Beclin-1)和 dynamin 相关蛋白 1(Drp-1):结果:模型组血尿素氮(BUN)和肌酐(SCr)的表达水平明显高于假手术组,表明建模成功。SSR 可通过减少肌酸激酶心肌同工酶和超敏心肌肌钙蛋白 I 的相对表达来保护心肌:5/6 肾切除 CKD 心肌损伤大鼠心肌组织中的 PINK1/Parkin 线粒体自噬途径受到抑制。SSR可激活PINK1/Parkin线粒体自噬,增强线粒体自噬,对心肌组织起到保护作用。
{"title":"Effect of phosphatase and tensin homolog-induced putative kinase 1/ E3 ubiquitin ligase Parkin mediated mitochondrial autophagy on chronic kidney disease myocardial injury and the intervention mechanism of Shenshuai recipe.","authors":"Zhang Gedi, Liu Gengxin, Guo Min, Luo Fuli, Yan Ziyou, G E Wei","doi":"10.19852/j.cnki.jtcm.20231231.001","DOIUrl":"10.19852/j.cnki.jtcm.20231231.001","url":null,"abstract":"<p><strong>Objective: </strong>To study whether Shenshuai recipe (, SSR) can play a protective role on chronic kidney disease myocardial injury model through phosphatase and tensin homolog-induced putative kinase 1 (PINK1)/E3 ubiquitin ligase Parkin (Parkin) mitochondrial autophagy pathway.</p><p><strong>Methods: </strong>Forty-eight nephrectomized rats were randomly divided into six groups: sham-operated group, model group, Benazepril group, low, medium and high-dose groups of SSR. The rats were given the cor-responding intervention for six weeks, then were sacrificed. Serum was examined by enzyme linked immunosorbent assay (ELISA). Cardiac ultrasound was used to detect cardiac function in 5/6 nephrectomized rats. Myocardial tissue was examined by light and electron microscopy; PINK1, Parkin, microtubule-associated protein1 light chain 3 II (LC3B), sequestosome 1 (P62), BECN1 (Beclin-1) and dynamin-related protein 1 (Drp-1) were measured by real time polymerase chain reaction (RT-PCR), Western blot (WB) and immunohistochemistry (IHC).</p><p><strong>Results: </strong>The expression levels of blood urea nitrogen (BUN) and creatinine (SCr) in the model group were significantly higher than those in the sham-operated group, indicating that modeling was successful. SSR can protect myocardium by reducing the relative expression of creatine kinase myocardial isoenzyme and hypersensitivity cardiac troponin I (<i>P</i><0.05). SSR can improve cardiac function in rats after ultrasound testing. SSR can improve the pathological manifestations of myocardial tissue after Masson staining. SSR can increase the number of autophagosomes and autophagiclysosomes in 5/6 nephrectomized rats (<i>P</i><0.05). Determined by RT-PCR, WB and IHC, SSR can increase the relative expression of PINK1, Parkin, and LC3B (<i>P</i><0.05), and decrease the relative expression of P62, Beclin-1 and Drp-1 (<i>P</i><0.05).</p><p><strong>Conclusions: </strong>The PINK1/Parkin mitochondrial autophagy pathway in myocardial tissues in 5/6 nephrectomy CKD myocardial injury rats was inhibited. SSR can activate PINK1/Parkin mitochondrial autophagy to enhance mitochondrial autophagy, and play a protective role in myocardial tissues.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":"44 5","pages":"934-943"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11462534/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142396428","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
Huaiyu pill alleviates inflammatory bowel disease in mice blocking toll like receptor 4/ myeloid differentiation primary response gene 88/ nuclear factor kappa B subunit 1 pathway. 怀牛膝丸通过阻断收费样受体 4/髓系分化主要反应基因 88/核因子卡巴 B 亚基 1 通路,缓解小鼠的炎症性肠病。
Pub Date : 2024-10-01 DOI: 10.19852/j.cnki.jtcm.20240719.001
Yang Chunyan, Luo Jia, Peng Weijie, Dai Weibo

Objective: To investigate the therapeutic effects of Huaiyu pill (, HYP) on inflammatory bowel disease (IBD) and the underlying mechanisms have not been elucidated.

Methods: To establish the IBD model, mice were administered with dextran sulfate sodium (DSS). Mice were intragastrically pre-treated with sulfasalazine (SASP) and HYP. Disease activity index (DAI) and colon length were monitored, and the colonic tissues were subjected to hematoxylin-eosin staining. Pro-inflammatory factors and vascular inflammation-related proteins were determined using enzyme-linked immunosorbent assay (ELISA). The potential mechanisms of HYP were examined using network pharmacology analysis.The expressions of zona occludens 1 (ZO-1), occludin, toll like receptor 4 (TLR4), myeloid differentiation primary response gene 88 (MYD88), and nuclear factor kappa B p65 subunit (NF-κB p65) in colon tissues were examined using Western blotting or immunohistochemical analyses.

Results: Pre-treatment with HYP enhanced the colon length, decreased DAI scores, and mitigated histopathological alterations in DSS-treated mice. HYP alleviated intestinal inflammation by downregulating the levels of interleukin 1 beta (IL-1β), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α) and interleukin 17 (IL-17). Additionally, HYP suppressed the disruption of the gut barrier by upregulating the ZO-1, occludin, and mucin 2 (MUC2) levels and downregulating the endothelin 1 (ET-1) and erythropoietin (EPO) levels. Network pharmacological analysis and experimental results revealed that HYP downregulated the colonic tissue levels of TLR4, MYD88, and NF-κB p65 in DSS-treated mice.

Conclusion: This study investigated the in vivotherapeutic effects of HYP on IBD and the underlying molecular mechanisms. These findings provide an experimental foundation for the clinical application of HYP.

目的研究怀牛膝丸(HYP)对炎症性肠病(IBD)的治疗作用及其机制:为了建立 IBD 模型,给小鼠注射右旋糖酐硫酸钠(DSS)。方法:为建立 IBD 模型,给小鼠注射硫酸右旋糖酐钠(DSS),并预先在胃内注射磺胺沙拉嗪(SASP)和 HYP。监测疾病活动指数(DAI)和结肠长度,并对结肠组织进行苏木精-伊红染色。使用酶联免疫吸附试验(ELISA)测定了促炎因子和血管炎症相关蛋白。使用 Western 印迹法或免疫组化分析法检测了结肠组织中闭孔带 1(ZO-1)、闭孔素、类收费受体 4(TLR4)、髓样分化主要反应基因 88(MYD88)和核因子卡巴 B p65 亚基(NF-κB p65)的表达情况:结果:用 HYP 预处理可增加 DSS 处理小鼠的结肠长度、降低 DAI 评分并减轻组织病理学改变。HYP 通过下调白细胞介素 1 beta(IL-1β)、白细胞介素 6(IL-6)、肿瘤坏死因子α(TNF-α)和白细胞介素 17(IL-17)的水平缓解了肠道炎症。此外,HYP 还通过上调 ZO-1、闭塞素和粘蛋白 2 (MUC2) 的水平以及下调内皮素 1 (ET-1) 和促红细胞生成素 (EPO) 的水平来抑制肠道屏障的破坏。网络药理学分析和实验结果表明,HYP 可下调 DSS 处理小鼠结肠组织中 TLR4、MYD88 和 NF-κB p65 的水平:本研究探讨了 HYP 对 IBD 的活体治疗作用及其分子机制。这些发现为 HYP 的临床应用提供了实验基础。
{"title":"Huaiyu pill alleviates inflammatory bowel disease in mice blocking toll like receptor 4/ myeloid differentiation primary response gene 88/ nuclear factor kappa B subunit 1 pathway.","authors":"Yang Chunyan, Luo Jia, Peng Weijie, Dai Weibo","doi":"10.19852/j.cnki.jtcm.20240719.001","DOIUrl":"10.19852/j.cnki.jtcm.20240719.001","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the therapeutic effects of Huaiyu pill (, HYP) on inflammatory bowel disease (IBD) and the underlying mechanisms have not been elucidated.</p><p><strong>Methods: </strong>To establish the IBD model, mice were administered with dextran sulfate sodium (DSS). Mice were intragastrically pre-treated with sulfasalazine (SASP) and HYP. Disease activity index (DAI) and colon length were monitored, and the colonic tissues were subjected to hematoxylin-eosin staining. Pro-inflammatory factors and vascular inflammation-related proteins were determined using enzyme-linked immunosorbent assay (ELISA). The potential mechanisms of HYP were examined using network pharmacology analysis.The expressions of zona occludens 1 (ZO-1), occludin, toll like receptor 4 (TLR4), myeloid differentiation primary response gene 88 (MYD88), and nuclear factor kappa B p65 subunit (NF-κB p65) in colon tissues were examined using Western blotting or immunohistochemical analyses.</p><p><strong>Results: </strong>Pre-treatment with HYP enhanced the colon length, decreased DAI scores, and mitigated histopathological alterations in DSS-treated mice. HYP alleviated intestinal inflammation by downregulating the levels of interleukin 1 beta (IL-1β), interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α) and interleukin 17 (IL-17). Additionally, HYP suppressed the disruption of the gut barrier by upregulating the ZO-1, occludin, and mucin 2 (MUC2) levels and downregulating the endothelin 1 (ET-1) and erythropoietin (EPO) levels. Network pharmacological analysis and experimental results revealed that HYP downregulated the colonic tissue levels of TLR4, MYD88, and NF-κB p65 in DSS-treated mice.</p><p><strong>Conclusion: </strong>This study investigated the <i>in vivo</i>therapeutic effects of HYP on IBD and the underlying molecular mechanisms. These findings provide an experimental foundation for the clinical application of HYP.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":"44 5","pages":"916-925"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11462535/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142396430","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
Electroacupuncture inhibits hippocampal oxidative stress and autophagy in sleep-deprived rats through the protein kinase B and mechanistic target of rapamycin signaling pathway. 电针通过蛋白激酶B和雷帕霉素机制靶点信号通路抑制睡眠不足大鼠的海马氧化应激和自噬作用
Pub Date : 2024-10-01 DOI: 10.19852/j.cnki.jtcm.20240806.002
Zheng Peng, Meng Ying, Liu Meijun, Y U Di, Liu Huiying, Wang Fuchun, X U Xiaohong

Objective: To investigate the effects of acupuncture on learning and memory impairment, oxidative stress and autophagy induced by sleep depriv ation in rats, and to analyze the related mechanism.

Methods: Thirty Wistar rats were randomly divided into a normal group, sleep deprivation group and acupuncture group. The rat model of sleep deprivation was established by a modified multiplatform sleep deprivation method. The Baihui (GV20), Shenmen (HT7) and Sanyinjiao (SP6) acupoints of rats were located to give electroacupuncture (density wave, frequency 20 Hz, intensity 1 mA) to maintain the needle feeling, and to keep the needle for 15 min and continuous acupuncture for 7 d. The spatial learning and memory abilities of the rats were detected by the water maze test. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPX) in the brain were detected by an assay kit, and the autophagy related proteins light chain 3 alpha (LC3A), light chain 3 beta (LC3B) and Beclin 1 and the activation of the protein kinase B (PKB/AKT) and mechanistic target of rapamycin (mTOR) signaling pathway in the rat's brain were detected by Western blotting.

Results: Compared with the normal group, the time spent in the target quadrant (P < 0.05) and the number of times entering the target quadrant (P < 0.05) in the rats of sleep deprivation group were significantly reduced, and the content of MDA was significantly increased (P < 0.01), while the activities of SOD and GPX (P < 0.01) in the brain were significantly decreased, and LC3A Ⅱ/Ⅰ, LC3B Ⅱ/Ⅰ and Beclin 1 increased significantly (P < 0.01), while p-AKT (ser473)/AKT, p-mTOR (ser2448)/mTOR and p-p70s6K (thr389)/p70S6 decreased significantly (P < 0.01). Compared with the sleep deprivation group, the time spent in the target quadrant and the times of entering the target quadrant (P < 0.05) in the rats of acupuncture group after 7 d of treatment were significantly increased, Additionally, the content of MDA was significantly decreased (P < 0.05), while the activities of SOD and GPX (P < 0.05) in the brain were significantly increased. Moreover, the levels of LC3A Ⅱ/Ⅰ, LC3BⅡ/Ⅰ and Beclin 1 decreased significantly (P < 0.05), and that of p-AKT (ser473)/AKT, p-mTOR (ser2448)/mTOR and p-p70s6K (thr389)/p70s6k increased significantly (P < 0.05).

Conclusion: Acupuncture can significantly improve the learning and memory damage caused by sleep deprivation and inhibit oxidative stress and autophagy, and its effect is related to the activation of AKT/mTOR signaling.

目的研究针灸对睡眠剥夺诱导的大鼠学习记忆障碍、氧化应激和自噬的影响,并分析其相关机制:方法:将 30 只 Wistar 大鼠随机分为正常组、睡眠剥夺组和针刺组。采用改良的多平台睡眠剥夺法建立大鼠睡眠剥夺模型。大鼠的百会穴(GV20)、神门穴(HT7)和三阴交穴(SP6)定位电针(密度波,频率20 Hz,强度1 mA),保持针感,留针15 min,连续针刺7 d。用检测试剂盒检测大鼠脑内丙二醛(MDA)的含量、超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GPX)的活性,以及自噬相关蛋白轻链3α(LC3A)、轻链3β(LC3B)和轻链3β(LC3C)的含量、轻链 3 beta(LC3B)和 Beclin 1,以及蛋白激酶 B(PKB/AKT)和雷帕霉素机械靶标(mTOR)信号通路的激活情况。结果显示与正常组相比,睡眠剥夺组大鼠在目标象限停留的时间(P 0.05)和进入目标象限的次数(P 0.05)明显减少,MDA含量明显升高(P 0.01),脑内SOD和GPX活性(P 0.01)明显降低,LC3A Ⅱ/Ⅰ、LC3B Ⅱ/Ⅰ和Beclin 1明显升高(P 0.01),p-AKT(ser473)/AKT、p-mTOR(ser2448)/mTOR和p-p70s6K(thr389)/p70S6明显降低(P 0.01)。与睡眠剥夺组相比,针刺组大鼠治疗7 d后在目标象限停留的时间和进入目标象限的次数(P 0.05)均明显增加,MDA含量明显降低(P 0.05),脑内SOD和GPX活性明显增加(P 0.05)。此外,LC3A Ⅱ/Ⅰ、LC3BⅡ/Ⅰ和Beclin 1的水平明显下降(P 0.05),p-AKT(ser473)/AKT、p-mTOR(ser2448)/mTOR和p-p70s6K(thr389)/p70s6k的水平明显升高(P 0.05):结论:针灸能明显改善睡眠剥夺导致的学习和记忆损伤,抑制氧化应激和自噬,其作用与AKT/mTOR信号的激活有关。
{"title":"Electroacupuncture inhibits hippocampal oxidative stress and autophagy in sleep-deprived rats through the protein kinase B and mechanistic target of rapamycin signaling pathway.","authors":"Zheng Peng, Meng Ying, Liu Meijun, Y U Di, Liu Huiying, Wang Fuchun, X U Xiaohong","doi":"10.19852/j.cnki.jtcm.20240806.002","DOIUrl":"10.19852/j.cnki.jtcm.20240806.002","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the effects of acupuncture on learning and memory impairment, oxidative stress and autophagy induced by sleep depriv ation in rats, and to analyze the related mechanism.</p><p><strong>Methods: </strong>Thirty Wistar rats were randomly divided into a normal group, sleep deprivation group and acupuncture group. The rat model of sleep deprivation was established by a modified multiplatform sleep deprivation method. The Baihui (GV20), Shenmen (HT7) and Sanyinjiao (SP6) acupoints of rats were located to give electroacupuncture (density wave, frequency 20 Hz, intensity 1 mA) to maintain the needle feeling, and to keep the needle for 15 min and continuous acupuncture for 7 d. The spatial learning and memory abilities of the rats were detected by the water maze test. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPX) in the brain were detected by an assay kit, and the autophagy related proteins light chain 3 alpha (LC3A), light chain 3 beta (LC3B) and Beclin 1 and the activation of the protein kinase B (PKB/AKT) and mechanistic target of rapamycin (mTOR) signaling pathway in the rat's brain were detected by Western blotting.</p><p><strong>Results: </strong>Compared with the normal group, the time spent in the target quadrant (<i>P <</i> 0.05) and the number of times entering the target quadrant (<i>P <</i> 0.05) in the rats of sleep deprivation group were significantly reduced, and the content of MDA was significantly increased (<i>P <</i> 0.01), while the activities of SOD and GPX (<i>P <</i> 0.01) in the brain were significantly decreased, and LC3A Ⅱ/Ⅰ, LC3B Ⅱ/Ⅰ and Beclin 1 increased significantly (<i>P <</i> 0.01), while p-AKT (ser473)/AKT, p-mTOR (ser2448)/mTOR and p-p70s6K (thr389)/p70S6 decreased significantly (<i>P <</i> 0.01). Compared with the sleep deprivation group, the time spent in the target quadrant and the times of entering the target quadrant (<i>P <</i> 0.05) in the rats of acupuncture group after 7 d of treatment were significantly increased, Additionally, the content of MDA was significantly decreased (<i>P <</i> 0.05), while the activities of SOD and GPX (<i>P <</i> 0.05) in the brain were significantly increased. Moreover, the levels of LC3A Ⅱ/Ⅰ, LC3BⅡ/Ⅰ and Beclin 1 decreased significantly (<i>P <</i> 0.05), and that of p-AKT (ser473)/AKT, p-mTOR (ser2448)/mTOR and p-p70s6K (thr389)/p70s6k increased significantly (<i>P <</i> 0.05).</p><p><strong>Conclusion: </strong>Acupuncture can significantly improve the learning and memory damage caused by sleep deprivation and inhibit oxidative stress and autophagy, and its effect is related to the activation of AKT/mTOR signaling.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":"44 5","pages":"974-980"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11462537/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142396429","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
Network-based pharmacology and experimental validation to explore the mechanism of action of the Jiawei Pentongling formula for the treatment of endometriosis-related pain. 基于网络药理学和实验验证,探索加味五通灵方治疗子宫内膜异位症相关疼痛的作用机制。
Pub Date : 2024-10-01 DOI: 10.19852/j.cnki.jtcm.20240806.004
Y U Siyun, Zhang Shiwen, Xia Yu, Liu Xiaoqing, Liu Yajie, F U Jinrong

Objective: To investigate the effects and mechanisms of the Jiawei Pentongling formula (, JWPTL) in treating endometriosis-related pain using network pharmacology study and experimental validation.

Methods: Active ingredients and relevant targets of JWPTL, as well as genes for endometriosis-related pain, were collected from public databases. Prediction of core targets and pathways of JWPTL against pain associated with endometriosis by protein-protein interaction (PPI) network work, gene ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analysis. The Sprague-Dawley rat endo-metriosis model was constructed using the autologous endosomal transplantation method, and the successfully modeled rats were randomly divided into the model group and the JWPTL group, with 8 rats in each group. Another 8 rats were set up in the sham group. Rats in the JWPTL group used the rectal delivery method with the addition of JWPTL (7.77 g·kg-1·d-1) once a day for 28 d. Rats in the model and sham-operated groups were given equal amounts of saline using the same administration method. The 50% paw withdrawal threshold (PWT) of the rats was measured at different time points. After the intervention, the expression of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt) proteins and mRNA in endometriotic tissues was detected by immune-ohistochemistry and reverse transcription-polymerase chain reaction.

Results: From GeneCards, Online Mendelian Inheritance in Man and other databases, a total of 964 endometriosis (EMs) -related pain targets were screened, 142 active ingredients of JWPTL, 605 targets, and 221 potential targets were obtained by intersection of Venn diagram; 44 core targets were identified by constructing PPI network. KEGG enrichment analysis showed that JWPTL mainly involves the PI3K-Akt signaling pathway, estrogen signaling pathway, hypoxia inducible factor-1 signaling pathway, tumour necrotizing factor signaling pathway, and other signaling pathways in the treatment of EMs-related pain. Animal experiments showed that JWPTL could up-regulate the mechanical pain threshold and reduce the expression of PI3K and Akt proteins and mRNA in ectopic endometrial tissues of model rats.

Conclusions: The present study preliminarily analyzed the pharmacological mechanism of the formula, and molecular docking and animal experiments showed the feasibility of this study, suggesting that the formula may inhibit the release of inflammatory factors and reverse the pain associated with EMs by downregulating the PI3K/Akt signaling pathway.

目的通过网络药理学研究和实验验证,探讨加味五通灵方(JWPTL)治疗子宫内膜异位症相关疼痛的作用和机制:方法:从公共数据库中收集加味五通灵方的有效成分、相关靶点以及子宫内膜异位症相关疼痛基因。通过蛋白-蛋白相互作用(PPI)网络工作、基因本体(GO)和京都基因组百科全书(KEGG)功能富集分析,预测 JWPTL 对抗子宫内膜异位症相关疼痛的核心靶点和通路。利用自体内膜移植法构建了Sprague-Dawley大鼠内膜异位症模型,并将成功建模的大鼠随机分为模型组和JWPTL组,每组8只。另设 8 只大鼠为假组。JWPTL组大鼠采用直肠给药法,添加JWPTL(7.77 g-kg-1-d-1),每天一次,持续28天;模型组和假手术组大鼠采用相同的给药方法,给予等量的生理盐水。在不同的时间点测量大鼠 50%的爪退缩阈值(PWT)。干预后,通过免疫组织化学和反转录聚合酶链反应检测子宫内膜组织中磷脂酰肌醇3-激酶(PI3K)和蛋白激酶B(Akt)蛋白和mRNA的表达:从GeneCards、Online Mendelian Inheritance in Man等数据库中筛选出与子宫内膜异位症(EMs)相关的疼痛靶点964个,其中JWPTL有效成分142个,靶点605个,通过维恩图交叉得到221个潜在靶点;通过构建PPI网络确定了44个核心靶点。KEGG富集分析表明,JWPTL在治疗电磁相关疼痛中主要涉及PI3K-Akt信号通路、雌激素信号通路、缺氧诱导因子-1信号通路、肿瘤坏死因子信号通路等信号通路。动物实验表明,JWPTL能上调模型大鼠异位子宫内膜组织的机械痛阈,降低PI3K和Akt蛋白及mRNA的表达:本研究初步分析了该方剂的药理机制,分子对接和动物实验表明了该研究的可行性,提示该方剂可通过下调PI3K/Akt信号通路,抑制炎症因子的释放,逆转EMs相关疼痛。
{"title":"Network-based pharmacology and experimental validation to explore the mechanism of action of the Jiawei Pentongling formula for the treatment of endometriosis-related pain.","authors":"Y U Siyun, Zhang Shiwen, Xia Yu, Liu Xiaoqing, Liu Yajie, F U Jinrong","doi":"10.19852/j.cnki.jtcm.20240806.004","DOIUrl":"10.19852/j.cnki.jtcm.20240806.004","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the effects and mechanisms of the Jiawei Pentongling formula (, JWPTL) in treating endometriosis-related pain using network pharmacology study and experimental validation.</p><p><strong>Methods: </strong>Active ingredients and relevant targets of JWPTL, as well as genes for endometriosis-related pain, were collected from public databases. Prediction of core targets and pathways of JWPTL against pain associated with endometriosis by protein-protein interaction (PPI) network work, gene ontology (GO), and Kyoto Encyclopedia of Genes and Genomes (KEGG) functional enrichment analysis. The Sprague-Dawley rat endo-metriosis model was constructed using the autologous endosomal transplantation method, and the successfully modeled rats were randomly divided into the model group and the JWPTL group, with 8 rats in each group. Another 8 rats were set up in the sham group. Rats in the JWPTL group used the rectal delivery method with the addition of JWPTL (7.77 g·kg<sup>-1</sup>·d<sup>-1</sup>) once a day for 28 d. Rats in the model and sham-operated groups were given equal amounts of saline using the same administration method. The 50% paw withdrawal threshold (PWT) of the rats was measured at different time points. After the intervention, the expression of phosphatidylinositol 3-kinase (PI3K) and protein kinase B (Akt) proteins and mRNA in endometriotic tissues was detected by immune-ohistochemistry and reverse transcription-polymerase chain reaction.</p><p><strong>Results: </strong>From GeneCards, Online Mendelian Inheritance in Man and other databases, a total of 964 endometriosis (EMs) -related pain targets were screened, 142 active ingredients of JWPTL, 605 targets, and 221 potential targets were obtained by intersection of Venn diagram; 44 core targets were identified by constructing PPI network. KEGG enrichment analysis showed that JWPTL mainly involves the PI3K-Akt signaling pathway, estrogen signaling pathway, hypoxia inducible factor-1 signaling pathway, tumour necrotizing factor signaling pathway, and other signaling pathways in the treatment of EMs-related pain. Animal experiments showed that JWPTL could up-regulate the mechanical pain threshold and reduce the expression of PI3K and Akt proteins and mRNA in ectopic endometrial tissues of model rats.</p><p><strong>Conclusions: </strong>The present study preliminarily analyzed the pharmacological mechanism of the formula, and molecular docking and animal experiments showed the feasibility of this study, suggesting that the formula may inhibit the release of inflammatory factors and reverse the pain associated with EMs by downregulating the PI3K/Akt signaling pathway.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":"44 5","pages":"991-999"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11462540/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142396432","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
Comprehensive review on ethnomedicinal, phytochemistry and pharmacological profile of. 全面综述了罂粟的民族药用价值、植物化学和药理学特征。
Pub Date : 2024-10-01 DOI: 10.19852/j.cnki.jtcm.2024.05.012
Rahul Rawat, Harish Kumar, Neetu Singh, Aakash Deep, Balasubramanian Narasimhan, Surender Singh Yadav, Sanjiv Kumar

Ficus religiosa L. (F. religiosa) or sacred fig is a large perennial tree belonging to the family Moraceae or mulberry family. Though the tree has pan-tropical distribution but originally it is indigenous to the Indian subcontinent and Indochina region. Popularly the tree is named "Pepal or bodhi tree". Traditionally, it is practiced for the treatment of asthma, nose bleeding, heart disorders, diabetes, wound healing, ear problems, constipation, hyperlipidemia, gonorrhea, ulcers and infectious disorders. Chemical analysis demonstrated the presence of numerous bioactives including tannins, phenols, saponins, sugars, alkaloids, methionine, terpenoids, flavonoids, glycosides, proteins, separated amino acids, essential and volatile oils and steroids etc., which are probably responsible for its diverse pharmacological actions. The present work is an attempt to compile up-to-date comprehensive information on F. religiosa that covers its taxonomy, ethnomedicinal importance, phytochemistry, pharmacological attributes and clinical trials. Keeping in mind the various health attributes of F. religiosa, future research can be aimed at in-depth elucidation of the structure-function relationship and multifactorial signalings pathways.

宗教无花果(Ficus religiosa L.)或神圣无花果是一种多年生大乔木,属于桑科(Moraceae)桑属。虽然这种树分布在泛热带地区,但最初是印度次大陆和印度支那地区的原生植物。这种树俗称 "Pepal 或菩提树"。传统上,它被用来治疗哮喘、鼻出血、心脏疾病、糖尿病、伤口愈合、耳疾、便秘、高脂血症、淋病、溃疡和传染病。化学分析显示,它含有大量生物活性物质,包括单宁酸、酚类、皂苷、糖类、生物碱、蛋氨酸、萜类、黄酮类、苷类、蛋白质、分离氨基酸、必需油和挥发油以及类固醇等,这些物质可能是它具有多种药理作用的原因。本研究试图编纂有关宗教草的最新综合信息,内容涵盖其分类、民族药用重要性、植物化学、药理特性和临床试验。考虑到 F. religiosa 的各种健康特性,未来的研究可以深入阐明其结构-功能关系和多因素信号通路。
{"title":"Comprehensive review on ethnomedicinal, phytochemistry and pharmacological profile of.","authors":"Rahul Rawat, Harish Kumar, Neetu Singh, Aakash Deep, Balasubramanian Narasimhan, Surender Singh Yadav, Sanjiv Kumar","doi":"10.19852/j.cnki.jtcm.2024.05.012","DOIUrl":"10.19852/j.cnki.jtcm.2024.05.012","url":null,"abstract":"<p><p><i>Ficus religiosa L.</i> (<i>F. religiosa</i>) or sacred fig is a large perennial tree belonging to the family Moraceae or mulberry family. Though the tree has pan-tropical distribution but originally it is indigenous to the Indian subcontinent and Indochina region. Popularly the tree is named \"Pepal or bodhi tree\". Traditionally, it is practiced for the treatment of asthma, nose bleeding, heart disorders, diabetes, wound healing, ear problems, constipation, hyperlipidemia, gonorrhea, ulcers and infectious disorders. Chemical analysis demonstrated the presence of numerous bioactives including tannins, phenols, saponins, sugars, alkaloids, methionine, terpenoids, flavonoids, glycosides, proteins, separated amino acids, essential and volatile oils and steroids etc., which are probably responsible for its diverse pharmacological actions. The present work is an attempt to compile up-to-date comprehensive information on <i>F. religiosa</i> that covers its taxonomy, ethnomedicinal importance, phytochemistry, pharmacological attributes and clinical trials. Keeping in mind the various health attributes of <i>F. religiosa</i>, future research can be aimed at in-depth elucidation of the structure-function relationship and multifactorial signalings pathways.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":"44 5","pages":"1052-1057"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11462526/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142396426","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
Systematic review and Meta-analysis of brain plasticity associated with electroacupuncture in experimental ischemic stroke. 实验性缺血性中风中电针相关脑可塑性的系统回顾和元分析。
Pub Date : 2024-10-01 DOI: 10.19852/j.cnki.jtcm.20240828.008
X U Yingshan, W U Chunxiao, Y U Wei, Guo Hongji, L U Liming, X U Nenggui, Tang Chunzhi

Objective: To systematically evaluate the role of electroacupuncture in maintaining brain plasticity in ischemic stroke mediated brain damage.

Methods: We searched for all relevant trials published through Oct 7, 2022 from seven databases. Metho-dological quality was assessed using the CAMARADES Risk of Bias Tool. A Meta-analysis of comparative effects was performed using Review Manager v.5.3 software.

Results: A total of 101 studies involving 2148 animals were included. For most studies, primary outcomes results of the Meta-analysis indicate that EA significantly improved ischemic stroke rat's postsynaptic density thickness [Standardized Mean Difference (SMD) = 1.41, 95% confidence interval (CI) (0.59, 2.23), P = 0.0008], numerical density of synapses [SMD = 1.55, 95% CI (0.48, 2.63), P = 0.005] compared with non-EA-treated. Similarly, EA could improve parts of biomarkers of synapses, neurogenesis, angiogenesis and neurotrophin activity than the control group (P < 0.05).

Conclusion: The existing evidence suggests EA regulating ischemic stroke may be through brain plasticity. More rigorous and high quality studies should be conducted in the future.

目的:系统评估电针在缺血性中风引起的脑损伤中维持脑可塑性的作用:系统评估电针在缺血性中风介导的脑损伤中维持脑可塑性的作用:我们从七个数据库中检索了截至 2022 年 10 月 7 日发表的所有相关试验。使用 CAMARADES 偏倚风险工具评估方法学质量。使用Review Manager v.5.3软件对比较效应进行了元分析:共纳入 101 项研究,涉及 2148 只动物。对于大多数研究,Meta 分析的主要结果显示,与非 EA 治疗相比,EA 能显著改善缺血性中风大鼠突触后密度厚度[标准化平均差(SMD)= 1.41,95% 置信区间(CI)(0.59,2.23),P = 0.0008]、突触数值密度[SMD = 1.55,95% CI(0.48,2.63),P = 0.005]。同样,与对照组相比,EA能改善突触、神经发生、血管生成和神经营养素活性等生物标志物的部分指标(P 0.05):现有证据表明,EA 可通过大脑可塑性调节缺血性中风。结论:现有证据表明,EA 可通过脑可塑性调节缺血性中风,未来应开展更严格、更高质量的研究。
{"title":"Systematic review and Meta-analysis of brain plasticity associated with electroacupuncture in experimental ischemic stroke.","authors":"X U Yingshan, W U Chunxiao, Y U Wei, Guo Hongji, L U Liming, X U Nenggui, Tang Chunzhi","doi":"10.19852/j.cnki.jtcm.20240828.008","DOIUrl":"10.19852/j.cnki.jtcm.20240828.008","url":null,"abstract":"<p><strong>Objective: </strong>To systematically evaluate the role of electroacupuncture in maintaining brain plasticity in ischemic stroke mediated brain damage.</p><p><strong>Methods: </strong>We searched for all relevant trials published through Oct 7, 2022 from seven databases. Metho-dological quality was assessed using the CAMARADES Risk of Bias Tool. A Meta-analysis of comparative effects was performed using Review Manager v.5.3 software.</p><p><strong>Results: </strong>A total of 101 studies involving 2148 animals were included. For most studies, primary outcomes results of the Meta-analysis indicate that EA significantly improved ischemic stroke rat's postsynaptic density thickness [Standardized Mean Difference (<i>SMD</i>) = 1.41, 95% confidence interval (<i>CI</i>) (0.59, 2.23), <i>P =</i> 0.0008], numerical density of synapses [<i>SMD</i> = 1.55, 95% <i>CI</i> (0.48, 2.63), <i>P =</i> 0.005] compared with non-EA-treated. Similarly, EA could improve parts of biomarkers of synapses, neurogenesis, angiogenesis and neurotrophin activity than the control group (<i>P <</i> 0.05).</p><p><strong>Conclusion: </strong>The existing evidence suggests EA regulating ischemic stroke may be through brain plasticity. More rigorous and high quality studies should be conducted in the future.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":"44 5","pages":"859-870"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11462533/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142396440","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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