摘要
目的 :探讨ATP敏感性K+ 通道 (KATP)开放剂吡那地尔 (pinacidil,Pin)对缺氧缺糖再复氧损伤大鼠大脑皮层神经细胞的保护作用。方法 :体外培养大鼠大脑皮层神经细胞 ,细胞培养至 10d ,建立神经细胞缺氧缺糖损伤模型 ,观察Pin及KATP阻断剂格列苯脲对缺氧缺糖不同时间 ,再复氧 2 4h后细胞死亡率、丙二醛 (MDA)含量、超氧化物歧化酶 (SOD)活力的影响。结果 :缺氧缺糖、再复氧后大鼠的神经细胞死亡率均显著升高、MDA生成增多、SOD的活力下降 ,Pin干预后 ,细胞死亡率下降、MDA生成减少、SOD的活力升高 ;格列苯脲能拮抗Pin这种保护作用。结论 :Pin对缺氧缺糖损伤神经细胞具有保护作用 。
Objective: To investigate the protective effects of ATP sensitive potassium channel (K ATP ) opener Pinacidil on glucose oxygen deprived injury in cultured cortical neurons in newborn rats. Methods: When primary cultured neurons were exposed to glucose oxygen deprived condition for 4,8,16 h,reoxygen 24 h,the percentage of cell death and content of malonicaldehyde(MDA) and superoxide dimutase(SOD) were measured. Results: Pinacidil (10 -6 mol·L -1 ) reduced the percentage of cell death. It also prevented the elevation of MDA and increased the activities of SOD. K ATP agonist Glibenclamide could prevent the protective effects of Pinacidil. Conclusion: These results suggest that K ATP opener has neuronal protective effect,partly because it can suppress the generation of lipid peroxide and increase the activities of antioxidant enzymes.
出处
《武汉大学学报(医学版)》
CAS
2003年第3期258-261,T001,共5页
Medical Journal of Wuhan University