【摘要】 目的观察白杨素对机械性创伤(MT)引起的大鼠继发性心肌损伤的保护作用,并探究其机制。方法将大鼠分为对照组、创伤组、创伤给药组(注射白杨素)和创伤溶剂组(注射DMSO),每组5只。检测左心室舒缩压力;TUNEL检测心肌细胞凋亡;MTT比色法检测细胞增殖;ELISA检测肿瘤坏死因子α(TNF-α)表达量;DCFH-DA法测定活性氧(ROS)数量;激光共聚焦显微镜观察心肌细胞内Ca2+浓度。结果与对照组相比,创伤组血流动力学参数LVDP、MAP、+d P/d Tmax和-d P/d Tmax均显著下降(P<0.01);心肌细胞凋亡指数显著上升(P<0.01);TNF-α诱导细胞炎性反应下细胞存活率明显下降(P<0.01);TNF-α含量和ROS水平均上升(P<0.01)。而白杨素组相比于创伤组,心功能各指标均显著上升(P<0.01);心肌细胞凋亡指数显著下降(P<0.01);TNF-α诱导细胞炎性反应下细胞存活率明显上升(P<0.01);TNF-α含量和ROS水平均下降(P<0.01)。结论 MT导致心肌损伤时白杨素通过抑制TNF-α和ROS的过量释放及细胞内钙超载,改善心肌细胞的凋亡而发挥心脏保护作用。更多还原

【Abstract】 Objective We are aimed at observing the protective effect of chrysin has on the mechanical traumatic( MT) rat heart,and exploring the mechanism. Methods Rats were randomly divided into control group,trauma group without treatment and trauma group with injection of chrysin or solvent DMSO,there were 5 rats in each group. The changes of the left ventricular diastolic pressure were recorded. By TUNEL staining,we assessed the apoptosis degree of cardiomyocytes. MTT assay was used to evaluate the proliferation of cells. ELISA was administered to identify the TNF-α level. DCFH-DA was used to estimate the intracellular generation of ROS. We used confocal laser scanning microscope photoed fluorescent images to observe the cardiomyocytes to determine the changes of intracellular Ca2+. Results Compared with control,in trauma group,+d P/d Tmax,MAP,-d P/d Tmaxand LVDP were significantly decreased( P < 0. 01),the apoptosis index apparently increased( P < 0. 01). The survival rate of inflammatory cells induced by TNF-α was lower( P < 0. 01). There was a significant increase of TNF-α and ROS level( P < 0. 01). Compared with trauma group,in chrysin group,+ d P/d Tmax,MAP,-d P/d Tmaxand LVDP were significantly increased( P < 0. 01),the apoptosis index apparently decreased( P <0. 01) The survival rate of inflammatory cells induced by TNF-α was higher( P < 0. 01). And There was a significant decrease of TNF-α and ROS level( P < 0. 01). Conclusions Chrysin alleviates MT induced excessive release of TNF-α,ROS and intracellular calcium overload which will reduce the apoptosis of myocardial cells and protect the heart.更多还原