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《G蛋白偶聯(lián)膽汁酸受體1激活對高糖誘導(dǎo)小鼠心肌細(xì)胞肥大的影響.pdf》由會(huì)員上傳分享,免費(fèi)在線閱讀,更多相關(guān)內(nèi)容在學(xué)術(shù)論文-天天文庫。
1、山東醫(yī)藥2017年第57卷第1期·論著·G蛋白偶聯(lián)膽汁酸受體1激活對高糖誘導(dǎo)小鼠心肌細(xì)胞肥大的影響11211馮健,吳丹,陳旭昕,劉應(yīng)才,李家富(1西南醫(yī)科大學(xué)附屬醫(yī)院,四川瀘州646000;2中國人民解放軍海軍總醫(yī)院)摘要:目的探討G蛋白偶聯(lián)膽汁酸受體1(TGR5)激活對高糖誘導(dǎo)小鼠心肌細(xì)胞肥大的影響。方法原代培養(yǎng)小鼠心肌細(xì)胞,將細(xì)胞分為對照組、高糖組、高糖+INT-777(TGR5受體激動(dòng)劑)組、高糖+INT-777+TGR5shRNA(以TGR5干擾慢病毒包裝)組。采用圖像分析系統(tǒng)測定各組細(xì)胞表面積,通過RT-PCR及Wes
2、ternblotting方法檢測TGR5干擾慢病毒效率,RT-PCR檢測各組促肥大因子(心房鈉尿因子、β-肌球蛋白重鏈)mRNA表達(dá)變化。結(jié)果成功培養(yǎng)小鼠心肌細(xì)胞。與對照組比較,高糖組心肌細(xì)胞表面積及促肥大因子mRNA表達(dá)增加(P均<0.05)。激活TGR5后,由高糖導(dǎo)致的心肌細(xì)胞表面積及促肥大因子mRNA表達(dá)的增加受到抑制(P均<0.05)。與激活TGR5組比較,干擾TGR5基因后,心肌細(xì)胞表面積及促肥大因子mRNA表達(dá)明顯增加(P均<0.05)。結(jié)論激活TGR5受體可以抑制高糖誘導(dǎo)的心肌細(xì)胞肥大及促肥大因子mRNA表達(dá),可能
3、是糖尿病性心肌病重要的藥物治療靶點(diǎn)。關(guān)鍵詞:心肌細(xì)胞肥大;G蛋白偶聯(lián)膽汁酸受體;高糖誘導(dǎo);INT-777;心房鈉尿因子;β-肌球蛋白重鏈;小鼠doi:10.3969/j.issn.1002-266X.2017.01.001中圖分類號:R542.2文獻(xiàn)標(biāo)志碼:A文章編號:1002-266X(2017)01-0001-03EffectofG-protein-coupledbileacidreceptor1activationonhighglucose-inducedcardiomyocytehypertrophyinmice1FEN
4、GJian,WUDan,CHENXuxin,LIUYingcai,LIJiafu(1TheAffiliatedHospitalofSouthwestMedicalUniversity,Luzhou646000,China)Abstract:ObjectiveToinvestigatetheeffectofG-protein-coupledbileacidreceptor1(TGR5)receptoractivationonhighglucose-inducedcardiomyocytehypertrophyinmice.Meth
5、odsAfterprimarycultureofmousecardiomyocytes,thecellsweredividedintothecontrolgroup,highglucosegroup,highglucose+INT-777(theagonistofTGR5receptor)andhighglucose+INT-777+TGR5shRNAgroup.Imageanalysissystemwasusedfordeterminationofcellsurfacearea,RT-PCRandWesternblotting
6、wereusedtodetectthelentivirusefficiencyofTGR5interference,andtheexpressionofpro-hy-pertrophygeneswasdetectedbyRT-PCR.ResultsThemousecardiomyocytesweresuccessfullycultured.Comparedwiththecontrolgroup,cardiomyocytes'surfaceareaandpro-hypertrophygenemRNAexpressionincrea
7、sedinthehighglucosegroup(allP<0.05).TGR5activationinhibitedtheincreaseofcardiomyocytes'surfaceareaandpro-hypertrophygenemRNAexpressionwhichwasinducedbyhighglucose(allP<0.05).Comparedwithhighglucose+INT-777group,car-diomyocytes'surfaceareaandpro-hypertrophygenemRNAexp
8、ressionincreasedsignificantlyafterTGR5geneinterference(allP<0.05).ConclusionTGR5receptoractivationcaninhibitcardiomyocytehypertroph