截断逆挽方对慢加急性肝衰竭大鼠线粒体凋亡途径的影响 .pdfVIP

截断逆挽方对慢加急性肝衰竭大鼠线粒体凋亡途径的影响

目的动态观察截断逆挽方对慢加急性肝衰竭（ACLF）大鼠线粒体凋亡途径

的影响，探讨其作用机制。方法SPF级Wistar大鼠随机分为正常组、模型组和

截断逆挽方组，猪血清腹腔注射13周联合D-氨基半乳糖、脂多糖急性攻击建立

ACLF模型。截断逆挽方组在急性攻击前予截断逆挽方灌胃3d。各组大鼠于急

性攻击后4、8、12h平行取材。电镜观察肝细胞超微结构，免疫组化检测肝组

织细胞色素C（CytC）表达，Westernblot检测肝组织Bid蛋白表达。结果与正

常组比较，模型组4、8hCytC和Bid表达量增加、12h表达量减少（P＜0.05）；

与模型组比较，截断逆挽方组4、8hCytC和Bid表达量减少、12h表达量增加

（P＜0.05）。电镜观察显示，模型组大鼠肝细胞超微结构严重破坏，且程度逐渐

加深，而各时间点截断逆挽方组大鼠肝细胞超微结构损伤程度较模型组均有所减

轻。结论截断逆挽方可有效降低ACLF大鼠肝细胞的损伤程度，其作用机制可

能与阻断肝细胞线粒体凋亡途径有关。

Abstract：ObjectiveTodynamicallyobservetheeffectsofJieduanNiwan

Formulaonmitochondrialapoptoticpathwayinacute-on-chronicliverfailure

（ACLF）rats；TofurtherrevealthepossiblemechanismofJieduanNiwanFormula.

MethodsSPFWistarratswererandomlydividedintonormalgroup，modelgroup

andJieduanNiwangroup.13-weekporcineseruminjectionfollowedwith

D-galactosamineandlipopolysaccharidejointacuteattackwasusedtoestablished

ACLFmodelinallratsexceptfornormalgroup.RatsinJieduanNiwangroupwere

orallygivenJieduanNiwanFormulafor3daysbeforeacuteattack.Ratswere

sacrificedrespectivelyat4，8and12haftermodelswereestablished.The

expressionsofBid，CytochromeC（CytC）andhepatocyteultrastructurewere

detectedbyWesternblotmethod，immunohistochemicalanalysisandtransmission

electronmicroscope，respectively.ResultsComparedwithnormalgroup，thelevels

12h（P＜0.05）；however，thelevelsofCytCandBidinJieduanNiwangroup

werelowerthanthoseinmodelgroupat4and8hbuthigherat12h（P＜0.05）.The

ultrastructuresweresignificantlydamagedinmodelrats，whichseveritywas

escalatedthroughtime；inJieduanNiwangroup，thedegreeofinjurydecreasedat

eachtiming.ConclusionJieduanNiwanFormulacanefficientlyalleviatethe

hepatocytedamageinACLFrats，andthemechanismmightbeinvolvedinthe

inhibitionofthemitochondrialapoptoticpathway.Keywords：acute-on-chronic