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实验以低氧 3h后复氧期间心肌细胞的生存率和LDH的释放量为指标 ,观察Gi/o蛋白及其下游成分在低氧预处理 (hypoxicpreconditioning ,HP)心肌保护中的作用。与单纯低氧组相比 ,HP组 ( 2 5min低氧 +30min复氧作为HP)细胞生存率增高 ,LDH释放减少 (P <0 0 1)。用NEM预处理 ,能完全模拟HP的心肌细胞保护作用 ;而用PTX阻断Gi/o蛋白 ,或Forskolin和 8 Br cAMP预处理后 ,再给予HP及低氧 3h/复氧 1h ,则细胞生存率降低 ,LDH释放增加 (P <0 0 1) ;U 7312 2预处理后 ,细胞生存率和LDH释放量无差异 (P >0 0 5 )。结果提示 :Gi/o蛋白通过抑制AC ,减少第二信使cAMP的生成介导了HP的心肌保护作用。PLC可能不参与HP的心肌保护作用
The effects of Gi / o protein and its downstream components on myocardial protection during hypoxic preconditioning (HP) were observed using the survival rate of cardiomyocytes and LDH release during reoxygenation 3 h after hypoxia as an indicator. Compared with simple hypoxia group, HP group (25min hypoxia + 30min reoxygenation as HP) increased the cell survival rate and reduced the release of LDH (P <0.01). Pretreatment with NEM could completely simulate the cardioprotective effect of HP. However, pretreatment with PTX blocked Gi / o protein or Forskolin and 8 Br cAMP followed by HP and hypoxia for 3 h / reoxygenation for 1 h, the cell survival (P <0.01). After U7312 2 pretreatment, there was no difference in cell viability and LDH release (P> 0.05). The results suggest that Gi / o protein mediates the cardioprotection induced by HP by inhibiting AC and decreasing the production of cAMP in second messengers. PLC may not be involved in HP’s cardioprotection