缺氧后处理对成年大鼠心肌细胞缺氧复氧损伤的保护作用

摘要

Objective To investigate whether hypoxic postconditioning exerts protective effect a‐gainst hypoxia reoxygenation injury in adult rat cardiomyocytes and to study the mechanisms involved in the effect. Methods Male SD rats ,250~350 g ,were randomly divided into 3 groups which were normal group (NOR group) ,hypoxia reoxygenation group (H/R group) ,and hypoxic postcondition‐ing group (group HP). Mitochondrial membrane potential ,intracellular calcium fluorescence intensity were detected with laser confocal microscope. Protein expression of phosphorylated p38MAPK (p‐p38MAPK)was measured with WB method. Results Compared with NOR group ,MMP of H/R and HP group was significantly reduced (P<0. 05). MMP of HP group was higher than H/R group (P<0. 05). Compared with NOR group and HP group ,intracellular calcium fluorescence intensity of H/R group was significantly increased (P< 0. 01). There were no statistical significantly differences be‐tween NOR group and HP group in intracellular calcium fluorescence intensity. Compared with NOR group and HP group ,p‐p38MAPK expression of H/R group was significantly increased (P<0. 05). There were no statistical significantly differences between NOR group and HP group in p ‐p38MAPK expression. Conclusion Hypoxic postconditioning exerts protective effects against hypoxia reoxygen‐ation injury in adult rat myocardial cells. The mechanism may be related to down regulated p‐p38MAPK expression in myocardial cells ,inhibition of mitochondrial membrane potential in decline and suppressing calcium overload.%目的：通过建立成年大鼠心肌细胞缺氧复氧模型观察缺氧后处理的心肌保护机制。方法雄性SD大鼠，体质量250～350 g ，随机分为3组：正常组（NOR组）、缺氧组（H／R组）、缺氧后组（HP组）。采用激光共聚焦显微镜检测心肌细胞线粒体膜电位（mitochondrial membrane potential ， MMP）、细胞内钙离子荧光强度以及 Western blot方法测定磷酸化 p38丝裂原活化蛋白激酶（p‐p38MAPK）表达量。结果（1）与正常组比较，H／R组和 HP组 MMP显著降低（P＜0．05）；HP组MMP明显高于 H／R组（P＞0．05）；（2）与正常组和 HP组比较，H／R组细胞内钙离子荧光强度显著升高（P＜0．01）；HP组和正常组间差异无统计学意义（P＞0．05）；（3）与正常组和 HP组比较，H／R组p‐p38MAPK表达量显著升高（P＜0．05）；HP组和正常组间表达量差异无统计学意义（P＞0．05）。结论缺氧后处理可对缺氧复氧成年大鼠心肌细胞产生保护作用，其机制可能与下调心肌细胞p‐p38M A PK 表达量、抑制线粒体膜电位下降以及防止钙超载进而抑制凋亡有关。