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目的观察血管紧张素(1-7)[AT-(1-7)]和卡托普利预处理对糖尿病大鼠心功能的影响并探讨其可能机制。方法 SD大鼠分为糖尿病对照(DM)组、糖尿病AT-(1-7)处理(DM+AT)组、糖尿病卡托普利处理(DM+Cap)组。采用Langendorff离体心脏灌流系统检测心功能,心肌缺血20 min再灌注20 min后,检测心功能指标、心肌氧化应激水平、胶原总量、胶原交联及赖氨酰氧化酶(LOX)的表达水平。结果缺血再灌注后,DM组各心功能指标较基线明显下降,DM+AT组和DM+Cap组的左心室收缩末压(LVESP)和左心室压力上升最大变化速率(+dp/dt_(max))较基线明显下降(P<0.01),但左心室压力下降最大变化速率(—dp/dt_(max))未见明显降低(P>0.05)。与DM组比较,DM+AT组和DM+Cap组丙二醛(MDA)含量显著降低,超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)活力显著增高。DM+AT组和DM+Cap组心肌胶原交联百分率和LOX蛋白表达低于DM组。结论 AT-(1-7)和卡托普利预处理促进糖尿病大鼠离体心脏缺血后舒张功能的恢复,其机制可能与增强糖尿病大鼠心肌的抗氧化能力、抑制胶原交联、LOX降低有关。
Objective To investigate the effects of angiotensin (1-7) [AT- (1-7)] and captopril on cardiac function in diabetic rats and its possible mechanism. Methods SD rats were divided into diabetic group (DM), diabetic AT- (1-7) treated group (DM + AT) and diabetic captopril treated group (DM + Cap). Cardiac function was detected by Langendorff perfusion cardioplegia system. After 20 minutes reperfusion of myocardial ischemia for 20 min, cardiac function, myocardial oxidative stress, total collagen, collagen cross-linking and lysyl oxidase (LOX) The expression level. Results After reperfusion, the indexes of cardiac function in DM group were significantly lower than those in baseline. The changes of left ventricular end-systolic pressure (LVESP) and left ventricular pressure (+ dp / dt_) in DM + AT group and DM + Cap group max) decreased significantly compared with baseline (P <0.01), but the maximal rate of change of left ventricular pressure (-dp / dt max) was not significantly decreased (P> 0.05). Compared with DM group, the content of malondialdehyde (MDA) in DM + AT group and DM + Cap group decreased significantly and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) increased significantly. The percentage of myocardial collagen cross-linking and the expression of LOX protein in DM + AT group and DM + Cap group were lower than those in DM group. CONCLUSION: AT- (1-7) and captopril preconditioning can promote the recovery of diastolic function after isolated ischemia in diabetic rats. The mechanism may be related to the anti-oxidative ability of myocardium in diabetic rats and the inhibition of collagen crosslinking, LOX Lower related.