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背景:阿魏酸钠预处理能对心肌细胞产生保护作用并已在大鼠体外心脏和乳鼠心肌细胞水平得以证实,尚缺乏在成年大鼠心肌细胞水平上的研究。目的:探讨阿魏酸钠预处理对成年大鼠缺氧复氧心肌细胞的保护作用及其K+ATP通道机制。方法:用Langendorff系统灌流心脏,以胶原酶消化法分离纯化成年大鼠心肌细胞并给予模拟缺氧复氧液以及干预因素阿魏酸钠、K+ATP通道阻断剂格列本脲处理,随机分为6组:正常对照组、缺氧复氧组、缺氧预适应+缺氧复氧组、阿魏酸钠+缺氧复氧组、格列本脲+缺氧预适应+缺氧复氧组、格列本脲+阿魏酸钠+缺氧复氧组。结果与结论:①心肌细胞存活率:缺氧复氧组与对照组比较,细胞存活率明显降低(P<0.01);缺氧预适应+缺氧复氧组、阿魏酸钠+缺氧复氧组与缺氧复氧组比较,细胞存活率明显增高(P<0.01);格列本脲+缺氧预适应+缺氧复氧组、格列本脲+阿魏酸钠+缺氧复氧组与缺氧复氧组相比,差异无显著性意义,但明显高于缺氧预适应+缺氧复氧组(P<0.01)。②乳酸脱氢酶活性:各组间乳酸脱氢酶活性比较结果与心肌细胞存活率比较结果吻合。③透射电镜观察:缺氧复氧组心肌细胞线粒体明显肿胀,嵴消失或变形,细胞膜结构破坏,有核边聚现象;缺氧预适应+缺氧复氧组、阿魏酸钠+缺氧复氧组心肌细胞超微结构改变轻微,线粒体排列规则、大小均匀,嵴及内外膜清晰完整,核膜完整,较缺氧复氧组损伤明显减轻;格列本脲+缺氧预适应+缺氧复氧组、格列本脲+阿魏酸钠+缺氧复氧组心肌细胞超微结构改变与缺氧复氧组相似。结果可见阿魏酸钠预处理对成年大鼠心肌细胞具有药理性心肌缺血预适应保护作用且该作用可能与K+ATP通道有关。
BACKGROUND: Sodium ferulate preconditioning has protective effects on cardiomyocytes and has been demonstrated in rat cardiac and neonatal rat cardiomyocytes. However, studies on myocardial cell levels in adult rats are still lacking. Objective: To investigate the protective effect of sodium ferulate preconditioning on hypoxia-reoxygenation cardiomyocytes in adult rats and its mechanism of K + ATP channel. Methods: The heart was perfused with Langendorff system. The myocardial cells of adult rats were isolated and purified by collagenase digestion. Mice were treated with simulated hypoxia-reoxygenation solution and interventional agents sodium ferulate and K + ATP channel blocker glibenclamide The rats were divided into 6 groups: normal control group, hypoxia reoxygenation group, hypoxic preconditioning + hypoxia reoxygenation group, sodium ferulate + hypoxia reoxygenation group, glibenclamide + hypoxia preconditioning + hypoxia complex Oxygen group, glibenclamide + sodium ferulate + hypoxia-reoxygenation group. RESULTS AND CONCLUSION: Cardiomyocyte survival rate: Compared with the control group, the survival rate of cardiomyocytes in hypoxia-reoxygenation group was significantly lower (P <0.01); hypoxia preconditioning + hypoxia-reoxygenation group, sodium ferulate + hypoxia complex Compared with the hypoxia-reoxygenation group, the cell survival rate was significantly increased in the oxygen group (P <0.01), while that in the glibenclamide + hypoxia preconditioning + hypoxia-reoxygenation group Compared with hypoxia-reoxygenation group, oxygen group had no significant difference, but was significantly higher than hypoxia preconditioning + hypoxia-reoxygenation group (P <0.01). ② lactate dehydrogenase activity: lactate dehydrogenase activity between groups compared with the results of myocardial cell survival rate was consistent. ③ Transmission electron microscopy: Myocardial mitochondria in the anoxia-reoxygenation group were obviously swollen, the cristae disappeared or deformed, the cell membrane structure was disrupted, nucleus edge aggregation phenomenon; hypoxia preconditioning + hypoxia-reoxygenation group, sodium ferulate + hypoxia complex The changes of ultrastructure of myocardial cells in oxygen group were slight, the rules of mitochondria were arranged, the size was uniform, the cristae and inner and outer membrane were clear and complete, the nuclear membrane was intact, and the damage of mitochondria was more obvious than hypoxia and reoxygenation group; The ultrastructural changes of myocardial cells in reoxygenation group, glibenclamide + sodium ferulate + hypoxia-reoxygenation group were similar to those in hypoxia-reoxygenation group. The results showed pretreatment of sodium ferulate preconditioning myocardial cells in rats with pharmacological effects of myocardial ischemic preconditioning and the role may be related to K + ATP channels.