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中医杂志（英文版）
中医杂志（英文版）

Cao Hong-xin

季刊

0255-2922

info@journaljtcm.com;jtcm@188.com

010-64050201

100700

北京东直门内南小街16号

中医杂志（英文版）/Journal Journal of Traditional Chinese MedicineCSCDSCI
正式出版
收录年代

    Systematic review and Meta-analysis of brain plasticity associated with electroacupuncture in experimental ischemic stroke

    XU YingshanWU ChunxiaoYU WeiGUO Hongji...
    859-870页
    查看更多>>摘要：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.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Traditional Chinese Medicine in the treatment of recurrent respiratory tract infections in children:an overview of systematic reviews and Meta-analyses

    DENG YashengHAN SiyinXI LanhuaHUANG Hui...
    871-884页
    查看更多>>摘要：OBJECTIVE:To evaluate and summarise the evidence from published Meta-analyses/systematic reviews(MAs/SRs)of Traditional Chinese Medicine(TCM)in the treatment of recurrent respiratory tract infections(RRTIs)and to provide a scientific basis for the clinical treatment of RRTIs with TCM.METHODS:Studies were retrieved from Chinese and English databases including the China National Knowledge Infrastructure,Wanfang database,China Science and Technology Journal Database,SinoMed,PubMed,Web of Science,the Cochrane Library and EMbase from their establishment date to March 2023.Involved studies were screened,extracted,and evaluated for quality by two researchers independently.The a measurement tool to assess systematic reviews(AMSTAR)2 scale was used for methodological quality evaluation,as well as the preferred reporting items for systematic reviews and Meta-analyses(PRISMA)2020 statement for report quality evaluation,the risk of bias in systematic reviews(ROBIS)tool for risk of bias,and the grading of recommendations,assessment,development and evaluation(GRADE)quality assessment tool for evidence quality.RESULTS:Twenty MAs/SRs studies were included,including analyses of 274 original studies involving 38335 patients with RRTIs.The AMSTAR 2 scale evaluation results showed that 19 studies were of very low quality and one of moderate quality.The ROBIS evaluation results showed that 11 MAs/SRs were at high risk and nine at low risk of bias.The PRISMA 2020 report quality showed the included studies had scores between 23.5 and 35.5,among them one with high quality,17 with moderate quality and two with low quality.The GRADE system results showed that among 126 outcome indicators,only 17 had moderate quality of evidence,27 had low quality,82 had very low quality,and none had high quality.CONCLUSIONS:The MAs/SRs methodological quality of using TCM for treatment RRTIs is generally poor,the quality of reports as well as of evidence is generally low,and the risk of bias is high;therefore we should treat these results with caution.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    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(加味白头翁汤)in the treatment of ulcerative colitis

    WU TingtingYANG XinZHU HuipingGUO Jinwei...
    885-895页
    查看更多>>摘要：OBJECTIVE:To investigate the mechanism of the protective effect of modified Pulsatilla decoction(加味白头翁汤,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.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Actinidia chinensis polysaccharide interferes with the epithelial-mesenchymal transition of gastric cancer by regulating the nuclear transcription factor-KB pathway to inhibit invasion and metastasis

    ZHANG GuangshunXU XiaonanXU ChuyunLIAO Guanghui...
    896-905页
    查看更多>>摘要：OBJECTIVE:To investigate the mechanisms of the effect of Actinidia chinensis polysaccharide(ACPS)on the invasion and metastasis of gastric cancer cells.METHODS:BGC-823-Luc gastric cancer cells stably transfected with a luciferase gene were used to establish an insitutransplanted tumor mouse model.A live mouse imaging system was used to observe tumor growth,and hematoxylin and eosin staining was applied to analyze tissue histopathology.Transwell and scratch wound assays were performed to examine the invasive and migratory ability of BGC-823 cells.Immunofluorescence,confocal microscopy,immunohistochemistry,and Western blot assays were used to analyze the expressions of the nuclear transcription factor-κB(NF-κB)signaling pathway and epithelial-mesenchymal transition(EMT)-related proteins.RESULTS:ACPS significantly inhibited the growth of subcutaneously transplanted BGC-823-Luc gastric cancer tumors in nude mice and reduced inflammatory cell infiltration in tumor tissues.ACPS inhibited Epidermal Growth Factor-induced invasion,migration,and morphological changes in the cytoskeleton of BGC-823 cells.ACPS inhibited gastric cancer EMT and decreased the expression of matrix metallopeptidase 9,N-cadherin and p-NF-κB p65 in transplanted tumor tissues.ACPS inhibited the expression of matrix metalloproteinases and vascular adhesion factors in BGC-823 cells,promoted p65-NF-κB nuclear translocation,and regulated proteins associated with the NF-κB p65 pathway.CONCLUSIONS:ACPS inhibited gastric cancer invasion and metastasis both in vivo and in vitro,which evidenced the inhibition of gastric cancer EMT via regulating the NF-κB inflammatory pathway.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Weitiao No.3(微调3号方)enhances the efficacy of anti-programmed cell death protein-1 immunotherapy by modulating the intestinal microbiota in an orthotopic model of gastric cancer mice

    HUANG XiaonaLI YuzhenZHU ChenyangZHU Hengzhou...
    906-915页
    查看更多>>摘要：OBJECTIVE:To explore the effects of Weitiao No.3(微调3号方,WD-3)on anti-programmed cell death protein-1(PD-1)immunotherapy in gastric cancer(GC).METHODS:The intestinal microbiota was analyzed by 16S rDNA sequencing of fecal samples from three groups:healthy people(Health),GC patients(GC),and WD-3-treated GC patients(WD-3).Next,we established an orthotopic model of GC mice,which were treated with anti-PD-1,WD-3,or an inoculation of intestinal bacteria.Immune markers CD3,CD4,CD8,and forkhead box protein P3(FOXP3),and the cell proliferation marker Ki67,were evaluated by immunohistochemistry.Cell apoptosis in GC tumors was assessed by terminal-deoxynucleotidyl-transferase-mediated deoxyuridine triphosphate nick end labeling staining.Enzyme-linked immunosorbent assays(ELISAs)were performed to analyze the serum levels of the following cytokines in GC mice:tumor necrosis factor(TNF)-α,interleukin(IL)-2,IL-6,IL-10,interferon(IFN)-γ,and transforming growth factor(TGF)-β.RESULTS:Sequencing data showed that there were significant differences in the composition of the gut microbial community among the three human groups.The gut bacteria in the three groups mainly comprised the phyla Firmicutes,Proteobacteria,Bacteroidetes,and Actinobacteria.At the genus level,the relative abundances of Bifidobacterium and Coprococcus showed significant decreases in the GC group,and an obvious increase in the WD-3 group,compared with the Health group.Interestingly,the relative abundance of Saccharopolyspora was only detected in the WD-3 group.The results of in vivo experiments in GC mice showed that WD-3 or anti-PD-1 treatment increased the levels of CD3+,CD4+,and CD8+T cells,but decreased the levels of FOXP3+regulatory T cells.Furthermore,WD-3 or PD-1 antibody treatment inhibited proliferation and promoted apoptosis of GC tumor cells.ELISA analysis showed that WD-3 or PD-1 antibody treatment facilitated TNF-α,IL-2,and IFN-γ expression,while suppressing IL-6,IL-10,and TGF-β expression.Combination therapy with WD-3 and anti-PD-1 intensified all of these effects.CONCLUSION:WD-3 enhanced the immunotherapeutic efficacy of anti-PD-1 by modulating the intestinal microbiota in an orthotopic model of GC mice.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Huaiyu pill(槐榆片)alleviates inflammatory bowel disease in mice via blocking toll like receptor 4/myeloid differentiation primary response gene 88/nuclear factor kappa B subunit 1 pathway

    YANG ChunyanLUO JiaPENG WeijieDAI Weibo...
    916-925页
    查看更多>>摘要：OBJECTIVE:To investigate the therapeutic effects of Huaiyu pill(槐榆片,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 vivo therapeutic effects of HYP on IBD and the underlying molecular mechanisms.These findings provide an experimental foundation for the clinical application of HYP.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Protective effect of Zhizi Huangqi Shanzha formula(栀子黄芪山楂方)on aflatoxin poisoning in mice and its effect on intestinal flora

    SUN ChuanboXU GuangpeiJIANG PingHUANG Shipping...
    926-933页
    查看更多>>摘要：OBJECTIVE:To evaluate the protective effect of Zhizi Huangqi Shanzha formula(栀子黄芪山楂方,ZHSF)on aflatoxin-induced liver injury.METHODS:The protective effect of ZHSF on the aflatoxin-induced liver injury was evaluated by histological observation,blood cell analysis,evaluation of liver function and immunity,and gut microbiota analysis.RESULTS:ZHSF can significantly up-regulate the percentage of lymphocytes and eosinophils in the blood of Aflatoxin B1-intoxicated mice,down-regulate the levels of serum aspartate aminotransferase,alanine aminotransferase,and malondialdehyde,and recover the liver tissue structure.Aflatoxin poisoning induces a variation of the intestinal flora of mice,and ZHSF may recover the variation of intestinal flora induced by Aflatoxin B1.Cluster analysis showed that the intestinal flora of mice in the intervention group was more similar to that of the control group.Correlation analysis showed that Lachnospiraceae,Desulfovibrio,and Lactobacillus may be the key flora for the pharmacological effects of ZHSF.CONCLUSIONS:ZHSF may protect against aflatoxin-induced liver damage,improve immunity,and inhibit oxidative stress by regulating the composition and relative abundance of intestinal flora,which makes it a promising liver-protective candidate drug.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    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(肾衰方)

    ZHANG GediLIU GengxinGUO MinLUO Fuli...
    934-943页
    查看更多>>摘要：OBJECTIVE:To study whether Shenshuai recipe(肾衰方,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.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Neuroprotective effect of Naochuxue prescription(脑出血方)on intracerebral hemorrhage:inhibition of autophagy via downregulating high mobility group box-1

    JIN HongWANG XinnaWANG RuonanLI Jinjian...
    944-953页
    查看更多>>摘要：OBJECTIVE:To determine the molecular mechanisms underlying the neuroprotective effects of Naochuxue prescription(脑出血方,NCXP)in rats with intracerebral hemorrhage(ICH).METHODS:Sprague-Dawley rats were injected with collagenase to generate ICH models,which were then randomly divided into six groups,including control,sham,model,and three intervention groups.The intervention groups received different doses of NCXP(0.13,0.26,and 0.52 g/kg)daily for 10 d.High-performance liquid chromatography(HPLC)was used to analyze the chemical characteristics of NCXP.The neurobehavioral outcomes of the rats were evaluated using neurological deficit scores(Zea Longa 5)and the corner turn test.Pathomorphological changes in perihematomal tissues after ICH were observed using hematoxylin and eosin staining.Immunohistochemistry(IHC)was used to detect the inflammation expression of interleukin 6(IL-6)and toll-like receptor 4(TLR4).High mobility group box-1(HMGB1),Beclin1,microtubule-associated protein 1 light chain 3 beta(LC3),and sequestosome 1(p62)were detected using real-time quantitative polymerase chain reaction and Western blotting in perihematomal tissues.RESULTS:HPLC showed that the NCXP had good stability.Rats with ICH had severe neurological function deficits compared to the control group.IHC results showed that NCXP significantly downregulated the expression of the inflammatory proteins IL-6 and TLR4.ICH rats treated with NCXP showed less neurological injury than the model group,accompanied by a significantly decreased expression of HMGB1,Beclin1,and LC3 and an increased expression of p62.CONCLUSIONS:The neuroprotective effect of NCXP alleviated inflammation and autophagy possibly by downregulating HMGB1 expression.However,further research on the signaling pathways is required to verify this hypothesis.
      原文链接:
    • NETL
    • NSTL
    • 万方数据

    Qingfei Zhisou oral liquid(清肺止嗽口服液)alleviates fever-induced inflammation by regulating arachidonic acid and lysophospholipids metabolism and inhibiting hypothalamus transient receptor potential ion channels expression

    GAO JiamingZHANG YehaoChen YuanyuanJIN Long...
    954-962页
    查看更多>>摘要：OBJECTIVE:To explore how Qingfei Zhisou oral liquid(清肺止嗽口服液,QFZS)adjusts body temperature bias and the interaction of inflammatory factors levels and metabolomic differences.METHODS:Dry yeast was subcutaneously injected at 10 mL/kg to establish the pyrexia model.We randomly divided 60 Sprague-Dawley rats into five groups:control,model,positive,low dose of QFZS and high dose of QFZS.Inflammatory proteins were evaluated by Western blotting and immunohistochemistry.For the examination of the endogenous metabolites,enzyme linked immunosorbent assay and ultra-high-performance liquid chromatography high-resolution mass spectrometry were employed.RESULTS:QFZS significantly reduced rats'body temperature within 6 h after dry yeast injection and reduced the secretion of the arginine vasopressin,cyclic adenosine monophosphate,prostaglandin E-2,tumor necrosis factor-α(TNF-α),interleukin-6(IL-6),and interleukin-1β in serum.Meanwhile,we identified 41 metabolites between the model and QFZS groups,including arachidonic acid and lysophospholipids.QFZS restored normal arachidonic acid levels.Based on the differential metabolite enrichment analysis,QFZS's anti-inflammatory and anti-pyrexia effects might be related to the inflammatory pathway regulated by transient receptor potential.Additionally,QFZS treatment reduced transient receptor potential melastatin 2 ion channel expression and affected TNF-α,heat shock protein 70,and cyclooxygenase-2 expression in the hypothalamus.CONCLUSION:QFZS exerts its regulatory effects on fever by regulating the metabolism of lysophospholipids and arachidonic acid and the regulation of inflammation via transient receptor potential ion channels channels.
      原文链接:
    • NETL
    • NSTL
    • 万方数据