中国药理学通报
中國藥理學通報
중국약이학통보
CHINESE PHARMACOLOGICAL BULLETIN
2014年
12期
1721-1724,1725
,共5页
林岩%肖薇%金莉%邓志会%李波%王国忠%刘吉成
林巖%肖薇%金莉%鄧誌會%李波%王國忠%劉吉成
림암%초미%금리%산지회%리파%왕국충%류길성
心肌肥大%内质网应激%白藜芦醇%细胞凋亡%GRP78%CHOP
心肌肥大%內質網應激%白藜蘆醇%細胞凋亡%GRP78%CHOP
심기비대%내질망응격%백려호순%세포조망%GRP78%CHOP
cardiac hypertrophy%endoplasmic reticu-lum stress%resveratrol%apoptosis%GRP78%CHOP
目的:探讨白藜芦醇(resveratrol,Res)对异丙肾上腺素(isoproterenol,ISO)诱导的心肌细胞肥大的保护作用及与内质网应激的关系。方法利用 ISO 建立乳鼠心肌肥大细胞模型,分为正常对照组、ISO 组,白藜芦醇干预组和白藜芦醇对照组。检测心肌细胞表面积和 ANP 基因表达;流式细胞仪检测细胞凋亡率;检测培养液中乳酸脱氢酶(LDH)和丙二醛(MDA)漏出量;实时定量 PCR 和 Western blot 分析GRP78和 CHOP 的基因和蛋白表达。结果Res 有效抑制ISO 诱导的心肌细胞肥大和凋亡,表现为降低心肌细胞表面积和 ANP 基因表达,减少 LDH、MDA 漏出量和心肌细胞凋亡率,同时下调 GRP78和 CHOP 的基因和蛋白表达。结论Res 可能通过抑制内质网应激相关因子 GRP78和 CHOP 表达发挥对心肌肥大的保护作用。
目的:探討白藜蘆醇(resveratrol,Res)對異丙腎上腺素(isoproterenol,ISO)誘導的心肌細胞肥大的保護作用及與內質網應激的關繫。方法利用 ISO 建立乳鼠心肌肥大細胞模型,分為正常對照組、ISO 組,白藜蘆醇榦預組和白藜蘆醇對照組。檢測心肌細胞錶麵積和 ANP 基因錶達;流式細胞儀檢測細胞凋亡率;檢測培養液中乳痠脫氫酶(LDH)和丙二醛(MDA)漏齣量;實時定量 PCR 和 Western blot 分析GRP78和 CHOP 的基因和蛋白錶達。結果Res 有效抑製ISO 誘導的心肌細胞肥大和凋亡,錶現為降低心肌細胞錶麵積和 ANP 基因錶達,減少 LDH、MDA 漏齣量和心肌細胞凋亡率,同時下調 GRP78和 CHOP 的基因和蛋白錶達。結論Res 可能通過抑製內質網應激相關因子 GRP78和 CHOP 錶達髮揮對心肌肥大的保護作用。
목적:탐토백려호순(resveratrol,Res)대이병신상선소(isoproterenol,ISO)유도적심기세포비대적보호작용급여내질망응격적관계。방법이용 ISO 건립유서심기비대세포모형,분위정상대조조、ISO 조,백려호순간예조화백려호순대조조。검측심기세포표면적화 ANP 기인표체;류식세포의검측세포조망솔;검측배양액중유산탈경매(LDH)화병이철(MDA)루출량;실시정량 PCR 화 Western blot 분석GRP78화 CHOP 적기인화단백표체。결과Res 유효억제ISO 유도적심기세포비대화조망,표현위강저심기세포표면적화 ANP 기인표체,감소 LDH、MDA 루출량화심기세포조망솔,동시하조 GRP78화 CHOP 적기인화단백표체。결론Res 가능통과억제내질망응격상관인자 GRP78화 CHOP 표체발휘대심기비대적보호작용。
Aim To explore the role of resveratrol (Res)on cardiomyocyte hypertrophy induced by iso-proterenol (ISO)and the relationship with endoplas-mic reticulum stress (ERS).Methods Hypertrophic model of cardiomyocytes was induced by ISO.Hyper-trophy status of cardiomyocytes was determined by measuring the cell surface area and the gene expression of ANP.The value of apoptosis was measured by flow cytometry,the content of LDH and MDA was measured in different groups,and the gene and protein expres-sions of GRP78 and CHOP were detected by real-time PCR and Western blot.Results Res could attentuate ISO-induced cardiomyocyte hypertrophy and apoptosis by reducing the cell surface area,the gene expression of ANP and the value of apoptosis.Res could inhibit ERS by downregulating the gene and protein expression of GRP78 and CHOP.Meanwhile,the content of LDH and MDA was decreased.Conclusions The results suggest that treatment of Res may protect cardiomyocyte hypertrophy,which is partially mediated by inhibiting the expression of ERS factors GRP78 and CHOP.