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目的探讨三磷酸腺苷(ATP)敏感性钾通道(KATP通道)在缺氧中对海马神经元的保护作用机制。方法比较对照组、单纯缺氧组、KATP通道激动剂+缺氧组、KATP通道阻断剂+缺氧组中神经元缺氧诱导因子1α亚基(HIF-1α)的蛋白表达、DNA断裂、以及神经元存活情况。结果试验持续8,12,24 h后,正常氧分压组细胞存活率为(100±0.98)%,缺氧8,12,24 h后,细胞的存活率分别降至(85.76±3.31)%,(80.13±1.76)%,(72.24±3.87)%,差异均有统计学意义(P<0.05);缺氧12,24 h后,缺氧+二氮嗪组细胞凋亡率分别为(8.1±3.1)%,(18.4±2.3)%,缺氧+甲糖宁组分别为(32.5±1.6)%,(45.7±3.4)%,与单纯缺氧组的(20.3±2.2)%,(31.6±1.7)%比较,差异均有统计学意义(P<0.05)。结论 KATP通道可以通过上调HIF-1α的蛋白表达水平,对缺氧中的海马神经元起到保护作用。
Objective To investigate the protective effect of ATP-sensitive potassium channel (KATP channel) on hippocampal neurons during hypoxia. Methods The protein expression of hypoxia inducible factor 1 alpha subunit (HIF-1α), DNA cleavage, DNA fragmentation in neurons in KATP channel blockers + hypoxia group and KATP channel blockers + hypoxia group were compared. As well as neuronal survival. Results After 8, 12 and 24 hours, the cell survival rate was (100 ± 0.98)% in normal oxygen pressure group and 85.76 ± 3.31% , (80.13 ± 1.76)% and (72.24 ± 3.87)%, respectively (P <0.05). The apoptotic rates of hypoxia + diazoxide group were (8.1 (32.5 ± 1.6)%, (45.7 ± 3.4)%, respectively, compared with those in hypoxia group (20.3 ± 2.2%) and (31.6 ± ± 1.7)%, the differences were statistically significant (P <0.05). Conclusion KATP channels can protect the hippocampal neurons from hypoxia by up-regulating the protein expression of HIF-1α.