目的探讨Intermedin1-53(IMD1-53)对败血症大鼠心脏的保护作用及可能的机制。方法雄性SD大鼠分成3组,对照组(8只),败血症组(8只),IMD组(6只),监测血流动力学指标,检测血糖和乳酸浓度;取心脏组织做TUNEL染色,免疫印迹法检测蛋白活化的cleaved caspase 3、Bax和Bcl-2的表达,测定IMD1-53对经典的盲肠结扎穿刺法诱导败血症大鼠的心肌细胞凋亡的影响。结果败血症组血流动力学指标平均动脉血压(MABP)、左心室内压最大上升速率(+LVdp/dtmax)、左心室内压最大下降速率(-LVdp/dtmax)绝对值、左心室收缩压(LVSP)显著低于对照组(均为P〈0.05)。TUNEL染色结果显示败血症组细胞凋亡、Cleaved caspase 3蛋白表达量显著高于对照组(均为P〈0.05),与败血症组相比,IMD组的上述指标均有显著改善(均为P〈0.05)。结论 IMD1-53可以保护败血症后期大鼠的心肌,显著改善心功能,其机制可能是抑制心肌细胞凋亡。
Objective To investigate the cardioprotective effects of interleukin1-53( IMD1-53) and its underlying mechanism in sepsis rats. Methods The SD rats were randomly assigned into 3 groups: control group( n = 8),sepsis group( n = 8),and IMD group( n = 6); the effect of IMD1-53 on the apoptosis of cardiomyocytes induced by classical cecal ligation was studied. The hemodynamic parameters were recorded through left common carotid catheterization,and plasma glucose and lactic acid levels were measured 20 hours after the surgery. Heart tissue was collected and subjected to TUNEL staining,and Western blotting was processed to assess the expression levels of cleaved caspase 3,Bax and Bcl2. Results The hemodynamic indexes in sepsis group such as mean arterial blood pressure( MABP),left ventricular peak rate of contraction( + LVdp/dtmax),absolute value of left ventricular peak rate of relaxation(-LVdp/dtmax),left ventricular systolic pressure( LVSP) were significantly lower than those in the control group( all P〈0. 05). TUNEL staining results showed that the apoptosis level of the cells and the expression of cleaved caspase 3 protein in sepsis group were significantly higher than those of control group( all P〈0. 05).Compared with sepsis group,the above indexes of IMD group were significantly improved( all P〈0. 05). In addition,TUNEL staining revealed lower degree of apoptosis after IMD1-53injection.Conclusions IMD1-53may protect myocardium and cardiac function of rats with late sepsis through inhibiting cardiomyocytes apoptosis.