Article(id=1292126413683974374, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.01.014, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1746633600000, receivedDateStr=2025-05-08, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785996543569, onlineDateStr=2026-08-06, pubDate=1768579200000, pubDateStr=2026-01-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785996543569, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785996543569, creator=13701087609, updateTime=1785996543569, updator=13701087609, issue=Issue{id=1292126377440989952, tenantId=1146029695717560320, journalId=1246415772164075586, year='2026', volume='42', issue='1', pageStart='1', pageEnd='147', issueExtLink='null', onlineDate='null', pubDate='1768579200000', pubDateStr='2026-01-17', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1785996534929, creator='13701087609', updateTime=1786014708731, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1292202603945947673, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1292202603950141978, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=86, endPage=92, ext={EN=ArticleExt(id=1292126415575605479, articleId=1292126413683974374, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Research of the effects of telmisartan on mice with viral myocarditis by
miR-320 based on PKNOX1/BCL10/MALT1 signaling pathway, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the effects of telmisartan tablets (Tel) on viral myocardialtis (VM) mice through microRNA-320 (miR-320) and its mechanism.
Methods A total of 60 BALB/c mice were divided into control group, model group, experimental group, Tel+rAAV-NC group and Tel+rAAV-miR-320 group, with 12 mice in each group. Except for control group, VM mouse models were established by intraperitoneal injection of coxsackievirus B3 0.1 mL containing 100 TCID50. Experimental group was given 10 mg·kg-1 Tel intragastrically for 7 days. Based on experimental group, rAAV-NC was injected into the tail vein (1×1011 viral copy number, dissolved in PBS 100 μL) in Tel+rAAV-NC group; based on experimental group, rAAV-miR-320 was injected into the tail vein (1×1011 viral copy number, dissolved in PBS 100 μL) in Tel+rAAV-miR-320 group. The relative expression levels of miR-320 were detected by quantitative real time polymerase chain reaction. Creatine kinase isoenzyme, myoglobin and troponin were detected by enzyme-linked immunosorbent assay. TdT-mediated dUTP nick end labeling was used to detect apoptosis. The relative expression levels of peroxiredoxin-like protein NOX1 (PKNOX1)/B-cell lymphoma 10 (BCL10)/mucosa associated lymphoid tissue lymphoma translocation gene 1 (MALT1) signaling pathway were detected by Western blot.
Results The relative expression levels of miR-320 in control group, model group, experimental group, Tel+rAAV-NC group and Tel+rAAV-miR-320 group were 1.00±0.18, 4.06±0.73, 1.82±0.34, 1.95±0.36 and 3.47±0.61, respectively; creatine kinase isoenzyme were (36.09±4.82), (125.18±19.67), (49.73±8.04), (55.62±8.25) and (103.56±17.49) U·mL-1, respectively; myoglobin were (72.35±11.46), (368.29±61.83), (93.62±15.27), (90.74±16.18) and (316.51±57.92) μg·L-1, respectively; troponin were (17.42±2.53), (64.74±10.90), (28.59±4.16), (32.45±5.98) and (53.91±9.64) μg·L-1, respectively; the apoptosis rates were (3.17±0.52)%, (28.46±5.39)%, (6.97±1.24)%, (8.01±1.53)% and (24.89±4.16)%, respectively; the relative expression levels of PKNOX1 protein were 1.00±0.15, 2.07±0.36, 1.43±0.19, 1.39±0.20 and 1.91±0.32, respectively; the relative expression levels of BCL10 protein were 1.00±0.18, 1.95±0.34, 1.48±0.22, 1.41±0.21 and 1.84±0.35, respectively; the relative expression levels of MALT1 protein were 1.00±0.13, 1.90±0.32, 1.26±0.15, 1.37±0.18 and 1.69±0.27, respectively. Statistical comparisons revealed significant differences between model group and control group, as well as between experimental group and model group, and between Tel+rAAV-miR-320 group and Tel+rAAV-NC group (all P<0.05).
Conclusion By inhibiting the expression of miR-320, Tel alleviates myocardial injury and inhibits apoptosis in VM mice, which may be achieved by inhibiting PKNOX1/BCL10/MALT1 signaling pathway.
, authors=Xiao-mei LUO, Yan-fei HU, Rong HAI, Wei WANG, Tao BO, authorsList=Xiao-mei LUO, Yan-fei HU, Rong HAI, Wei WANG, Tao BO, authorCompany=null, correspAuthors=Xiao-mei LUO, authorNote=null, correspAuthorsNote=null, copyrightStatement=null, copyrightOwner=null, extLink=null, articleAbsUrl=null, sourceXml=null, magXml=null, pdfUrl=null, pdf=null, pdfFileSize=null, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=null, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=null, mapNumber=null, fund=null), CN=ArticleExt(id=1292126415823069416, articleId=1292126413683974374, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=替米沙坦基于PKNOX1/BCL10/MALT1信号通路通过
miR-320对病毒性心肌炎小鼠作用的研究, columnId=1246531407485489349, journalTitle=中国临床药理学杂志, columnName=临床与基础桥接研究, runingTitle=null, highlight=null, articleAbstract=
目的 探讨替米沙坦片（Tel）通过微小RNA-320（miR-320）对病毒性心肌炎（VM）小鼠的作用及其机制。
方法 将60只BALB/c小鼠分为对照组、模型组、实验组、Tel+rAAV-NC组和Tel+rAAV-miR-320组，每组12只。除对照组外均通过腹腔注射含100 TCID50的柯萨奇B3病毒0.1 mL建构VM小鼠模型。实验组灌胃给予10 mg·kg-1 Tel，连续7 d；Tel+rAAV-NC组在实验组的基础上，尾静脉注射rAAV-NC（1×1011病毒拷贝数，溶于磷酸盐缓冲液100 μL）；Tel+rAAV-miR-320组在实验组的基础上，尾静脉注射rAAV-miR-320（1×1011病毒拷贝数，溶于磷酸盐缓冲液100 μL）。用实时定量反转录聚合酶链式反应法检测miR-320相对表达水平；用酶联免疫吸附试验法检测肌酸激酶同工酶、肌钙蛋白和肌红蛋白水平；用原位末端标记染色法检测细胞凋亡情况；用蛋白质印迹法检测过氧化物还原酶样蛋白NOX1（PKNOX1）/B-细胞淋巴瘤因子10（BCL10）/黏膜相关淋巴瘤转运蛋白1（MALT1）信号通路相关蛋白相对表达水平。
结果 对照组、模型组、实验组、Tel+rAAV-NC组和Tel+rAAV-miR-320组的miR-320相对表达水平分别为1.00±0.18、4.06±0.73、1.82±0.34、1.95±0.36和3.47±0.61；肌酸激酶同工酶分别为（36.09±4.82）、（125.18±19.67）、（49.73±8.04）、（55.62±8.25）和（103.56±17.49）U·mL-1；肌红蛋白分别为（72.35±11.46）、（368.29±61.83）、（93.62±15.27）、（90.74±16.18）和（316.51±57.92）μg·L-1；肌钙蛋白分别为（17.42±2.53）、（64.74±10.90）、（28.59±4.16）、（32.45±5.98）和（53.91±9.64）μg·L-1；细胞凋亡率分别为（3.17±0.52）%、（28.46±5.39）%、（6.97±1.24）%、（8.01±1.53）%和（24.89±4.16）%；PKNOX1蛋白的相对表达水平分别为1.00±0.15、2.07±0.36、1.43±0.19、1.39±0.20和1.91±0.32；BCL10蛋白的相对表达水平分别为1.00±0.18、1.95±0.34、1.48±0.22、1.41±0.21和1.84±0.35；MALT1蛋白的相对表达水平分别为1.00±0.13、1.90±0.32、1.26±0.15、1.37±0.18和1.69±0.27。模型组的上述指标与对照组比较，实验组的上述指标与模型组比较，Tel+rAAV-miR-320组的上述指标与Tel+rAAV-NC组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 Tel通过抑制miR-320表达，减轻VM小鼠心肌损伤，抑制细胞凋亡，这可能是通过抑制PKNOX1/BCL10/MALT1信号通路实现的。
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骆小梅（1978-），女，副主任医师，主要从事心血管内科专业和急诊内科专业方面的临床工作和研究
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