中国药理学通报
中國藥理學通報
중국약이학통보
CHINESE PHARMACOLOGICAL BULLETIN
2015年
2期
194-197,198
,共5页
血管紧张素Ⅱ%RIP140%PGC-1α%ATP%能量代谢%心肌细胞
血管緊張素Ⅱ%RIP140%PGC-1α%ATP%能量代謝%心肌細胞
혈관긴장소Ⅱ%RIP140%PGC-1α%ATP%능량대사%심기세포
angiotensin Ⅱ%receptor interacting pro-tein 140%peroxisome proliferator-activated receptor gamma coactivator-1α%ATP%energy metabolism%car-diomyocytes
目的：探讨转录辅助因子受体相互作用蛋白140( re-ceptor interacting protein 140, RIP140)与过氧化物酶体增殖物受体γ共激活因子1α( peroxisome proliferator-activated re-ceptor gamma coactivator-1α, PGC-1α)在血管紧张素Ⅱ( an-giotensin Ⅱ, AngⅡ)调节心肌细胞能量代谢中的作用。方法借助腺病毒载体系统诱导RIP140和PGC-1α基因过表达；利用荧光检测系统测定乳鼠心肌细胞线粒体ATP的含量；实时荧光定量PCR和Western blot的方法检测RIP140和PGC-1α的表达情况。结果乳鼠心肌细胞给予100 nmol· L-1 Ang Ⅱ刺激36 h后,心肌细胞线粒体ATP的含量降低(P<0．01),同时伴随RIP140 mRNA与蛋白水平的升高,而PGC-1αmRNA与蛋白水平下调。 AngⅡ诱导的ATP含量减少在过表达 RIP140组中进一步下降,而在过表达 PGC-1α组中有所减轻。结论 Ang Ⅱ诱导的 ATP 含量减少与RIP140表达上调和PGC-1α表达下调有关。
目的：探討轉錄輔助因子受體相互作用蛋白140( re-ceptor interacting protein 140, RIP140)與過氧化物酶體增殖物受體γ共激活因子1α( peroxisome proliferator-activated re-ceptor gamma coactivator-1α, PGC-1α)在血管緊張素Ⅱ( an-giotensin Ⅱ, AngⅡ)調節心肌細胞能量代謝中的作用。方法藉助腺病毒載體繫統誘導RIP140和PGC-1α基因過錶達；利用熒光檢測繫統測定乳鼠心肌細胞線粒體ATP的含量；實時熒光定量PCR和Western blot的方法檢測RIP140和PGC-1α的錶達情況。結果乳鼠心肌細胞給予100 nmol· L-1 Ang Ⅱ刺激36 h後,心肌細胞線粒體ATP的含量降低(P<0．01),同時伴隨RIP140 mRNA與蛋白水平的升高,而PGC-1αmRNA與蛋白水平下調。 AngⅡ誘導的ATP含量減少在過錶達 RIP140組中進一步下降,而在過錶達 PGC-1α組中有所減輕。結論 Ang Ⅱ誘導的 ATP 含量減少與RIP140錶達上調和PGC-1α錶達下調有關。
목적：탐토전록보조인자수체상호작용단백140( re-ceptor interacting protein 140, RIP140)여과양화물매체증식물수체γ공격활인자1α( peroxisome proliferator-activated re-ceptor gamma coactivator-1α, PGC-1α)재혈관긴장소Ⅱ( an-giotensin Ⅱ, AngⅡ)조절심기세포능량대사중적작용。방법차조선병독재체계통유도RIP140화PGC-1α기인과표체；이용형광검측계통측정유서심기세포선립체ATP적함량；실시형광정량PCR화Western blot적방법검측RIP140화PGC-1α적표체정황。결과유서심기세포급여100 nmol· L-1 Ang Ⅱ자격36 h후,심기세포선립체ATP적함량강저(P<0．01),동시반수RIP140 mRNA여단백수평적승고,이PGC-1αmRNA여단백수평하조。 AngⅡ유도적ATP함량감소재과표체 RIP140조중진일보하강,이재과표체 PGC-1α조중유소감경。결론 Ang Ⅱ유도적 ATP 함량감소여RIP140표체상조화PGC-1α표체하조유관。
Aim To investigate the role of transcrip-tional cofactors receptor interacting protein 140 ( RIP140 ) and peroxisome proliferator-activated recep-tor γ coactivator-1α ( PGC-1α) in the angiotensin Ⅱ( AngⅡ) mediated energy metabolism regulation in cardiomyocytes. Methods RIP140 or PGC-1α was overexpressed via adenovirus vector system. ATP con-tents were detected by luminescence detection assay system. Real-time PCR and Western blot analysis were used to measure the expressions of RIP140 and PGC-1α genes. Results After treated with 100 nmol·L-1 AngⅡfor 36h in neonatal cardiomyocytes, the content of mitochondrial ATP was reduced notably ( P <0. 01). Accordingly, the mRNA and protein levels for RIP140 were increased. However, the mRNA and pro-tein levels of PGC-1α were downregulated markedly. What’ s more,the reduction of ATP induced by AngⅡwas further aggravated by RIP 1 4 0 overexpression , but ameliorated by overexpressing PGC-1α. Conclusion The reduction of ATP mediated by AngⅡis associated with the upregulation of RIP140 , as well as the down-regulation of PGC-1α.
