CAJ | 학술논문

目的:探讨在心肌缺血/再灌注和腺苷诱导预适应过程中细胞膜钙泵(PMCA)的可能作用.方法:将培养的乳鼠心肌细胞分为3组:缺血/再灌注组、腺苷预处理组和对照组.各组乳酸脱氢酶(LDH)漏出量以生化法检测(n＝5);半定量RT-PCR检测各组PMCA基因转录水平(n＝3);PMCA活性以定磷比色法测定(n＝5).结果:(1)缺血/再灌注组LDH漏出量明显增高(P<0.001),腺苷预处理组LDH漏出量显著降低(P<0.001);(2)各组间PMCA mRNA转录水平无显著性差异(P>0.05);(3)各组间PMCA蛋白活性无显著性差异(P>0.05).结论:在乳鼠心肌细胞缺血/再灌注过程中PMCA无代偿功能;PMCA不直接参与腺苷诱导预适应的心肌保护作用.
목적:탐토재심기결혈/재관주화선감유도예괄응과정중세포막개빙(PMCA)적가능작용.방법:장배양적유서심기세포분위3조:결혈/재관주조、선감예처리조화대조조.각조유산탈경매(LDH)루출량이생화법검측(n＝5);반정량RT-PCR검측각조PMCA기인전록수평(n＝3);PMCA활성이정린비색법측정(n＝5).결과:(1)결혈/재관주조LDH루출량명현증고(P<0.001),선감예처리조LDH루출량현저강저(P<0.001);(2)각조간PMCA mRNA전록수평무현저성차이(P>0.05);(3)각조간PMCA단백활성무현저성차이(P>0.05).결론:재유서심기세포결혈/재관주과정중PMCA무대상공능;PMCA불직접삼여선감유도예괄응적심기보호작용.
Objective The plasma membrane calcium ATPase (PMCA) is a calcium extruding enzyme controlling calcium homeostasis in nonexcitable cells. However, its role in myocardium remain controversial. Against previous consideration that PMCA exert a fine adjustment on calcium transmembrne transport, Recent several experiments proved that the contribution of PMCA to the Ca2+ removal is significant and might play a compensate role in some pathophysiologic conditions. Therefore the object of this study was to investigate the alterations of gene transcription and protein activity of PMCA on the process of ischemia/reperfusion and adenosine-induced pharmacological preconditioning. Methods The cultured neonatal rat ventricular cardiomyocytes were subjected to 9 h simulated ischemia /1 h reperfusion (I/R); or the cells were pretreated with 10 μmol·L-1 adenosine for 1 h prior to I/R. The levels of PMCAs gene transcription were measured by semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) and the alternations of PMCA activity were determined by the mirocolorimetric method for inorganic phosphorus. Cell damage was indicated by lactate dehydrogenase (LDH) release assay. Results LDH release were elevated significantly after I/R (P<0.001), while in cardiomycytes pretreated with 10 μmol·L-1 adenosine for 1 h prior to I/R, LDH release were significantly lowered (P<0.001). There were no alterations of PMCA gene transcription and protein activity in the I/R process and the adenosine pretreatment group (all P>0.05). Conclusion PMCA has no compensate role in I/R and doesnt participate in adenosine-induced preconditioning in rat myocyte.