Article(id=1317125577363018581, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317125500041015883, articleNumber=null, orderNo=null, doi=10.13193/j.issn.1673-7717.2026.02.036, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=null, receivedDateStr=null, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1791956808653, onlineDateStr=2026-10-14, pubDate=1770652800000, pubDateStr=2026-02-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1791956808653, onlineIssueDateStr=2026-10-14, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1791956808653, creator=13701087609, updateTime=1791956808653, updator=13701087609, issue=Issue{id=1317125500041015883, tenantId=1146029695717560320, journalId=1255847919539208197, year='2026', volume='44', issue='2', pageStart='1', pageEnd='258', issueExtLink='null', onlineDate='null', pubDate='1770652800000', pubDateStr='2026-02-10', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1791956790217, creator='13701087609', updateTime=1791958795145, updator='13701087609', preIssue=null, nextIssue=null, articleTotal=null, ext={EN=IssueExt(id=1317133909368877755, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317125500041015883, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1317133909373072060, tenantId=1146029695717560320, journalId=1255847919539208197, issueId=1317125500041015883, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null, downloadFileDto=null}, startPage=211, endPage=214, ext={EN=ArticleExt(id=1317125577551762262, articleId=1317125577363018581, tenantId=1146029695717560320, journalId=1255847919539208197, language=EN, title=Total Flavonoids of Lizhihe(Lichi Semen)Inhibiting Hepatic Inflammasome Activation and Alleviating Hepatic Fibrosis in Rats, columnId=1256183361521967297, journalTitle=Chinese Archives of Traditional Chinese Medicine, columnName=Target on National Project, runingTitle=null, highlight=null, articleAbstract=
Objective To investigate the mechanism by which total flavonoids of Lizhihe(Lichi Semen)(TFL)inhibiting NLRP3 inflammasome activation and attenuating hepatic fibrosis in rats.
Methods Hepatic fibrosis in rats was caused by subcutaneous injection of 40% carbon tetrachloride(CCl4),and the rats were randomly divided into a blank group,a model group,a Fuzheng Huayu Capsule(扶正化瘀胶囊)group(450 mg/kg),a TFL high-dose group(180 mg/kg),a TFL medium-dose group(90 mg/kg)and a TFL low-dose group(45 mg/kg)according to their body weights. After 8 weeks of gavage administration,the fibrotic lesions of liver tissue were observed by Masson staining,and the levels of tissue inhibitor of metalloproteinase-1(TIMP-1),matrix metal oproteinase-2(MMP-2)and reactive oxygen species(ROS)in liver tissue were detected. The expressions of thioredoxin interacting protein(TXNIP),NOD-like receptor thermal protein domain associated protein 3(NLRP3),Caspase-1 and interleukin-1β(IL-1β)proteins in liver tissue were determined by Western blotting.
Results Each dose of TFL attenuated the degree of hepatic tissue fibrosis in rats and significantly reduced the hepatic fibrosis grade(P<0.05),and the hepatic tissue levels of TIMP-1 and MMP-2 were significantly decreased in each dose group of TFL(P<0.05). What's more,all doses of TFL significantly reduced the liver tissue ROS level(P<0.01),and decreased the expressions of TXNIP,Caspase-1 and IL-1β proteins(P<0.05).
Conclusion TFL significantly attenuated CCl4-induced hepatic fibrosis in rats,and the mechanism may be related to the reduction of hepatic ROS accumulation,which inhibits the activation of NLRP3 inflammatory vesicles.
, authors=Yinting TUO
1, Xinglan HU
1, Bocun LI
2, Weisheng LUO
1, Jinling ZHOU
1, 3, Xing XIA
1, 3, authorsList=Yinting TUO, Xinglan HU, Bocun LI, Weisheng LUO, Jinling ZHOU, Xing XIA, authorCompany=null, correspAuthors=null, 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=1317125578256405335, articleId=1317125577363018581, tenantId=1146029695717560320, journalId=1255847919539208197, language=CN, title=荔枝核总黄酮抑制肝脏炎症小体活化并减轻大鼠肝纤维化, columnId=1256183362172142382, journalTitle=中华中医药学刊, columnName=国家项目点击, runingTitle=null, highlight=null, articleAbstract=
目的 探索荔枝核总黄酮(Total flavonoids of Lichi Semen,TFL)抑制NLRP3炎症小体活化、抗大鼠肝纤维化的机制。
方法 以皮下注射40%四氯化碳(CCl4)造成大鼠肝纤维化模型,将大鼠按体质量随机分为空白组、模型组、扶正化瘀胶囊组(450 mg/kg)、TFL高剂量组(180 mg/kg)、TFL中剂量组(90 mg/kg)、TFL低剂量组(45 mg/kg)。灌胃给药8周后,Masson染色观察肝组织纤维化病变,并检测肝组织基质金属蛋白酶抑制剂-1(Tissue inhibitor of metall oproteinase-1,TIMP-1)、基质金属蛋白酶-2(Matrix metalloproteinase-2,MMP-2)以及活性氧(Reactive oxygen species,ROS)水平;以Western bolt测定肝组织硫氧还蛋白相互作用蛋白(Thioredoxin interacting protein,TXNIP)、NOD样受体热蛋白结构域相关蛋白3(NOD-like receptor thermal protein domain associated protein 3,NLRP3)、半胱天冬酶1(Caspase-1)、白细胞介素(Interleukin,IL)-1β蛋白的表达。
结果 TFL各剂量减轻了大鼠肝组织纤维化程度,显著降低肝纤维化分级(P<0.05),并且TFL各剂量组肝组织TIMP-1、MMP-2水平显著下降(P<0.05)。更重要的是,TFL各剂量均显著减少了肝组织ROS水平(P<0.01),且降低了TXNIP、Caspase-1、IL-1β蛋白表达(P<0.05)。
结论 TFL能显著减轻CCl4诱发的大鼠肝纤维化,其机制可能与减少肝脏ROS的积累,从而抑制NLRP3炎症小体的活化有关。
, authors=陀银婷
1, 胡兴兰
1, 李泊村
2, 罗伟生
1, 周金玲
1, 3, 夏星
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1.College of Pharmacy,Guangxi University of Chinese Medicine,Nanning 530200,Guangxi,China
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1.广西中医药大学药学院,广西南宁 530200
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