中文摘要：

本文旨在研究脂联素（adiponectin, APN）对缺氧/复氧（hypoxia/reoxygenation, H/R）损伤的心肌细胞T-钙黏蛋白（T-cadherin,T-cad）表达的影响。采用酶消化法原代培养Sprague-Dawley （SD）乳鼠心肌细胞,随机分为：正常对照组、H/R组、H/R＋脂联素（3, 10, 20, 30 μg/mL）组。H/R组置缺氧环境（高浓度N2饱和过的缺氧液）中培养3 h后, 再置于复氧环境（纯氧饱和过的复氧液）中培养1 h。APN处理组先用不同浓度APN预处理24 h后中随后处理同H/R组。用化学比色法测定乳酸脱氢酶（LDH）的释放,通过流式细胞术和脱氧核糖核苷酸缺口末端标记（TUNEL）法来检测心肌细胞的凋亡,用RT-PCR和Western blotting方法检测T-cad的表达。结果显示,与正常对照组相比,H/R组心肌细胞凋亡率显著升高,心肌细胞LDH的释放量明显增加,T-cadmRNA和蛋白水平表达均明显下降;而和H/R组相比,APN预处理可剂量依赖性地降低心肌细胞凋亡率,减少LDH释放量,并上调T-cad mRNA和蛋白水平。以上结果提示,脂联素可能通过上调T-cad的表达逆转H/R所致的心肌细胞损伤及凋亡,对心肌细胞有保护作用。

英文摘要：

The aim of the present study was to investigate the effects of adiponectin（APN） on the expression of T-cadherin in cultured Sprague-Dawley（SD） rat cardiomyocytes injured by hypoxia/reoxygenation（H/R）.Primary myocardial cells from neonatal rats were obtained by enzymatic digestion.The cells were divided into control group,H/R group and H/R＋APN（3,10,20 and 30 μg/mL） groups.The H/R group was incubated in anoxic environment（anoxic solution saturated with high concentration N 2） for 3 h,and then in the reoxygenation environment（the reoxygenation solution saturated with pure oxygen） for 1 h.The H/R＋APN group was pretreated with different concentrations of APN for 24 h prior to the initiation of H/R.The content of lactate dehydrogenase（LDH） was measured by chemistry chromatometry.Cellular apoptosis was analyzed by flow cytometry and terminal deoxynucleotidyl transferasemediated dUTP nick end labeling（TUNEL）.The expression of T-cadherin was detected by RT-PCR and Western blotting.The results showed that,compared with control group,the apoptotic rate and release of LDH were significantly increased in the H/R group,whereas the expressions of T-cad mRNA and protein were decreased.Pretreating with APN significantly and dose-dependently decreased apoptotic rate and LDH release,and up-regulated T-cad mRNA and protein level in rat neonatal cardiomyocytes under H/R conditions.These results suggest that APN may protect cardiomyocytes against H/R-induced injury by up-regulating H/R-decreased T-cad expression.