梔子苷通過SIRT1通路干預冠心病動脈粥樣硬化內(nèi)質(zhì)網(wǎng)應激的作用機制

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AbstractObjective：ToanalyzetheefectofgeniposideGE）onendoplasmicreticulumstress（ERs）incoronaryheartdiease atherosclerosistroughsilentinformationregulator1（SI1）pathwayMethods：VascularsmoothmusclecelsCs）weredividednto control group（Con），angiotensin（Ang II） group，GE group，and Ang π+GE group.The expressions of Cleaved Caspase-3，X-box binding protein 1（XBP-1），activating transcription factor 6（ATF-6），and ATF- ?6β proteins in VSMCscelswere analyzedby Western Blot.Terminal deoxynucleotidyltransferase-medateddUTPnickendlabelingTUNEL）stainingwasusedtodetectapoptosis，andimmunofluorescence wasusedtodetect SIRT1expression.Thirty-twomale ApoEmicewererandomlydivided intofourgroups（8miceineachgroup）： control group（Ctrl），Ang II group，GE group，and Ang I+GE group.The mice in GE group and AngI +GE group were given GE by gavageeverydayAttendofthexperimentalperiodaortictisuewasbtaindfrommicefoanalysisofapoptosisandEs： Compared with the Con group，the expression of cleaved Caspase-3，XBP1，and ATF- ?6β in the Ang II group up-regulated ?P<0.05 ，and thepercentageof TUNEL-positivecellsincreased significantly（ P<0.05 .Comparedwith the AngII group，the expression of Caspase-3， XBP1，and ATF- ?6β down-regulated ?P<0.05? ，andthe percentageof TUNEL-positivecellsdecreased significantly （P<0.05） .Inaddition， thefluorescence intensity of SiRT1 increased significantly （P<0.05 ）inthe AngII +GE group.Compared with the Ctrl group，the expressionof cleavedcaspase-3，XBP1，and ATF ?6β proteinsin theaortic intima of the AngII group up-regulated （P<0.05） ，and the percentage of TUNEL-positive tissues increased significantly（ P<0.05） .Compared with the Ang II group，the expression levels of Caspase-3，XBP1，and ATF- 6β proteins in the Ang I+GE groupdown-regulated （P<0.05） ，andthe percentageof TUNEL-positive tissues decreased significantly （P<0.05） .Compared with the AngI group，the fluorescence intensity of SiRT1 in the Ang I+GE group increased significantly（ P<0.05 .Conclusion： GE enhances the intervention of ERs in coronary atherosclerosis by changing SIRT1 signaling pathway，thus protecting VSMCs from apoptosis induced by Ang I.

Keywordscoronaryeartdisease；atherosrosis；geiposidesilentinfoatioregulatorpathaydoplasmicetclutrs; vascularsmoothmusclecells;experiment study

動脈粥樣硬化是心血管疾病的主要原因，包括冠狀動脈和外周動脈閉塞性疾病、主動脈瘤和腦卒中，也是全球人類健康的最大威脅之一[1]。（剩余10865字）