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目的 探讨ATP敏感性钾通道(KATP)开放剂吡那地尔(Pinacidil,Pin)对体外培养大鼠大脑皮层神经细胞缺氧缺糖损伤的保护作用。 方法 取培养10 d神经细胞,建立神经细胞缺氧缺糖损伤模型。实验分正常对照组、模型对照组、给药组(Pin和 Pin+Gli处理组),观察缺氧缺糖 4、8、16 h,再复氧24 h后神经细胞死亡率、乳酸脱氢酶(LDH)漏出量和细胞凋亡率的变化,并观察 Pin及KATP通道阻断剂格列苯脲(Gli)对其影响。 结果 经缺氧缺糖损伤后神经细胞死亡率、LDH%和细胞凋亡率均显著升高,Pin干预后,细胞死亡率(4 h: 21.42±3.68和14.83±2.94; 8 h: 36.58±6.14和19.25±3.33; 16 h: 49.17±8.3和28.64±6.4, P值均<0.01)、LDH%(4 h: 26.9±6.1和13.2±4.1; 8 h: 31.4±4.9和18.7±5.3; 16 h: 47.7±6.5和28.1±6.8, P值均<0.01)和细胞凋亡率(16 h: 42±7.8和20.4±5.5, P<0.01)均显著下降,Gli能对抗 Pin这种保护作用。 结论 KATP开放剂Pin具有直接的神经保护作用,其发挥保护作用的机制与其抑制神经细胞凋亡有关。
Objective To investigate the protective effect of pinacidil (Pinacidil), an ATP-sensitive potassium channel (KATP) opener, on the injury of cultured rat cerebral cortex neurons against oxygen-glucose deprivation. Methods Cultured neuronal cells for 10 days to establish a model of hypoxic-glucose deprivation injury in neurons. The experimental group was divided into normal control group, model control group and administration group (Pin and Pin + Gli treatment group). The neuronal cell death rate, lactate dehydrogenase (LDH) leakage and apoptosis rate changes, and observe Pin and KATP channel blocker glibenclamide (Gli) on its impact. Results After hypoxia / glucose deprivation injury, the rate of neuronal cell death, LDH% and apoptosis were significantly increased. After Pin intervention, the cell death rates (4 h: 21.42 ± 3.68 and 14.83 ± 2.94; 8 h: 36.58 ± 6.14 And 19.25 ± 3.33; 16 h: 49.17 ± 8.3 and 28.64 ± 6.4, P <0.01), LDH% (4 h: 26.9 ± 6.1 and 13.2 ± 4.1; 8 h: 31.4 ± 4.9 and 18.7 ± 5.3; : 47.7 ± 6.5 and 28.1 ± 6.8, both P <0.01) and apoptotic rate (16 h: 42 ± 7.8 and 20.4 ± 5.5, P <0.01), and Gli could antagonize the protective effect of Pin. Conclusion The KATP opener Pin has a direct neuroprotective effect, and its protective mechanism is related to the inhibition of neuronal apoptosis.