Pub Date : 2024-10-01DOI: 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.
{"title":"International standard of Traditional Chinese Medicine techniques: the operating specification for Traditional Chinese Medicine enema (2022).","authors":"Y U Miao, Pei Xiaohua","doi":"10.19852/j.cnki.jtcm.2024.05.010","DOIUrl":"10.19852/j.cnki.jtcm.2024.05.010","url":null,"abstract":"<p><p>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.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":"44 5","pages":"1035-1043"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11462528/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142396431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-01DOI: 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.
{"title":"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.","authors":"W U Tingting, Yang Xin, Zhu Huiping, Guo Jinwei, Zhu Hui, Zhang Peipei, Wang Meng, Liang Guoqiang, Sun Hongwen","doi":"10.19852/j.cnki.jtcm.20240806.006","DOIUrl":"10.19852/j.cnki.jtcm.20240806.006","url":null,"abstract":"<p><strong>Objective: </strong>To investigate the mechanism of the protective effect of modified Pulsatilla decoction (, MPD) on the mechanical barrier of the ulcerative colitis (UC) intestinal epithelium <i>in vitro</i> and <i>in vivo</i>.</p><p><strong>Methods: </strong>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 <i>in vivo</i> 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.</p><p><strong>Results: </strong>In <i>in vitro</i> 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.</p><p><strong>Conclusions: </strong>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.</p>","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":"44 5","pages":"885-895"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11462527/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142396436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-01DOI: 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
{"title":"A pilot study of precision treatment for patients with lung cancer pain by Longteng Tongluo recipe using serum genomics.","authors":"W U Ruixin, Fang Qingliang, Guan Sisi, Wei Xianglong, Shan Mengjun, Mao Zhujun, Gong Yabin, X U Ling, Zhou Di, Dong Changsheng","doi":"10.19852/j.cnki.jtcm.20240828.005","DOIUrl":"10.19852/j.cnki.jtcm.20240828.005","url":null,"abstract":"<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","PeriodicalId":94119,"journal":{"name":"Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan","volume":"44 5","pages":"1006-1016"},"PeriodicalIF":0.0,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11462530/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142396404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-10-01DOI: 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.
{"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}
Pub Date : 2024-10-01DOI: 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.
{"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}
Pub Date : 2024-10-01DOI: 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.
{"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}
Pub Date : 2024-10-01DOI: 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.
{"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}
Pub Date : 2024-10-01DOI: 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.
{"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}
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}
Pub Date : 2024-10-01DOI: 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.
{"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}