Article(id=1292126426321416689, tenantId=1146029695717560320, journalId=1246415772164075586, issueId=1292126377440989952, articleNumber=null, orderNo=null, doi=10.13699/j.cnki.1001-6821.2026.01.013, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1747324800000, receivedDateStr=2025-05-16, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1785996546582, onlineDateStr=2026-08-06, pubDate=1768579200000, pubDateStr=2026-01-17, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1785996546582, onlineIssueDateStr=2026-08-06, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1785996546582, creator=13701087609, updateTime=1785996546582, 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=81, endPage=85, ext={EN=ArticleExt(id=1292126426543714802, articleId=1292126426321416689, tenantId=1146029695717560320, journalId=1246415772164075586, language=EN, title=Reaserch of quercetin on myocardial ischemia reperfusion injury in rats by regulating TLR2/NLRP3 pathway, columnId=1246531407326105792, journalTitle=Chinese Journal of Clinical Pharmacology, columnName=Clinical and Basic Bridging Research, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the impact of quercetin (Que) on myocardial ischemia-reperfusion injury in rats and to elucidate its underlying mechanisms.
Methods A rat model of myocardial ischemia-reperfusion was created by occluding the left anterior descending artery. A total of 60 SD rats were randomly divided into sham group, model group, low-dose experimental group (20 mg·kg-1 Que), high-dose experimental group (80 mg·kg-1 Que) and inhibitor group (80 mg·kg-1 Que+3 mg·kg-1 MCC950), with 12 rats in each group. Echocardiography was conducted after 14 days of continuous administration to assess the relevant indicators of cardiac function. Rat serum was taken and the amounts of serum myocardial damage indicators and inflammatory factors were detected by kit method. Western blotting was used to determine the relative expression levels of Toll-like receptor 2 (TLR2)/ nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) - related proteins in the rat myocardial tissue.
Results The left ventricular ejection fraction of rats in sham group, model group, low-dose experimental group, high-dose experimental group and inhibitor group were (79.36±5.37)%, (42.85±3.96)%, (48.51±4.20)%, (71.66±5.14)% and (55.73±4.68)%, respectively; the troponin Ⅰ (cTnⅠ) levels were (0.07±0.01), (0.38±0.03), (0.25±0.03), (0.13±0.01) and (0.20±0.02) ng·mL-1, respectively; the interleukin-1β (IL-1β) levels were (1.01±0.15), (3.43±0.22), (2.65±0.26), (1.39±0.23) and (1.61±0.13) ng·mL-1, respectively; the relative expression levels of TLR2 protein were 0.33±0.05, 1.01±0.07, 0.73±0.05, 0.45±0.03 and 0.50±0.06, respectively; the relative expression levels of NLRP3 protein were 0.34±0.06, 1.05±0.09, 0.86±0.07, 0.39±0.06 and 0.56±0.05, respectively. Compared with sham group, the model group showed statistically significant differences in the above indicators (all P<0.05); compared with model group and high-dose experimental group, the low-dose experimental group also exhibited statistically significant differences in the above indicators (all P<0.05).
Conclusion Quercetin can alleviate myocardial ischemia-reperfusion (I/R) injury in rats and improve cardiac function. The mechanism may be related to the inhibition of the TLR2/NLRP3 inflammatory signaling pathway. Quercetin may exert its cardioprotective effect by down-regulating the expression of TLR2, thereby blocking its activation of the downstream NLRP3 inflammasome, containing NLRP3 and apoptosis-associated speck-like protein containing a CARD (ASC) and ultimately reducing the release of pro-inflammatory factors such as IL-1β.
, authors=Ting-ting ZHAO, Sheng JIANG, Shuai FENG, Xin-yu LIU, Yi-bo YANG, authorsList=Ting-ting ZHAO, Sheng JIANG, Shuai FENG, Xin-yu LIU, Yi-bo YANG, authorCompany=null, correspAuthors=Sheng JIANG, 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=1292126426807955955, articleId=1292126426321416689, tenantId=1146029695717560320, journalId=1246415772164075586, language=CN, title=槲皮素调控TLR2/NLRP3通路对大鼠心肌缺血再灌注损伤的研究, 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 探索槲皮素（Que）对大鼠心肌缺血再灌注损伤的影响及作用机制。
方法 用左前降支结扎法建立大鼠心肌缺血再灌注模型。将60只SD大鼠随机分为假手术组、模型组、低剂量实验组（20 mg·kg-1Que）、高剂量实验组（80 mg·kg-1 Que）和抑制剂组（80 mg·kg-1 Que+3 mg·kg-1 MCC950），每组12只。连续给药14天后行超声心动图检测心功能相关指标，收集大鼠血清用试剂盒法检测血清心肌损伤标志物及炎症因子水平；用蛋白质印迹法检测大鼠心肌组织TLR2/NLRP3相关蛋白相对表达水平。
结果 假手术组、模型组、低剂量实验组、高剂量实验组和抑制剂组大鼠的左室射血分数分别为（79.36±5.37）%、（42.85±3.96）%、（48.51±4.20）%、（71.66±5.14）%和（55.73±4.68）%，肌钙蛋白Ⅰ（cTnⅠ）含量分别为（0.07±0.01）、（0.38±0.03）、（0.25±0.03）、（0.13±0.01）和（0.20±0.02）ng·ml-1，白细胞介素1β（IL-1β）水平分别为（1.01±0.15）、（3.43±0.22）、（2.65±0.26）、（1.39±0.23）和（1.61±0.13）ng·ml-1，Toll样受体2（TLR2）蛋白相对表达水平分别为0.33±0.05、1.01±0.07、0.73±0.05、0.45±0.03和0.50±0.06，核苷酸结合寡聚化结构样受体3（NLRP3）蛋白相对表达水平分别为0.34±0.06、1.05±0.09、0.86±0.07、0.39±0.06和0.56±0.05。模型组的上述指标与假手术组比较，低剂量实验组上述指标与模型组和高剂量实验组比较，在统计学上差异均有统计学意义（均P<0.05）。
结论 槲皮素可以减轻大鼠心肌I/R损伤，改善心功能，其机制可能与抑制TLR2/NLRP3炎症信号通路有关。槲皮素可能通过下调TLR2表达，进而阻断其对下游NLRP3炎症小体的激活，包括NLRP3和凋亡相关斑点样蛋白（ASC），最终减少IL-1β等促炎因子的释放，从而发挥心保护作用。
, authors=赵婷婷, 姜胜, 冯帅, 刘心雨, 杨一波, authorsList=赵婷婷, 姜胜, 冯帅, 刘心雨, 杨一波, authorCompany=null, correspAuthors=姜胜, authorNote=
赵婷婷（1989-），女，副教授，主要从事冠心病相关的基础与临床工作
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