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目的 研究三磷酸腺苷敏感性钾通道 (KATP)在一氧化氮 (NO)对缺氧 /复氧心肌细胞损害中的保护作用。方法 采用细胞缺氧 /复氧损伤模型 ,培养细胞随机分为 5组 :A组 ,正常对照组(培养 3h) ;B组 ,格列本脲 (glybenclamide ,Gly ,商品名 :优降糖 )预处理组 ,加入终浓度为 10 μmol/LGly后培养 3h ;C组 ,单纯缺氧 /复氧组 (A/R缺氧 2h ,复氧 1h) ;D组 ,一氧化氮预处理组 ,加入S 亚硝基 已酰青酶胺 (S nitroso n acetyl penicillamine ,SNAP)使其终浓度为 1mmol/L ,预处理 4 0min后缺氧复氧 ;E组 ,Gly +SNAP预处理组 ,加入终浓度为 10 μmol/LGly ,培育 2 0min后再加入SNAP使其终浓度为 1mmol/L ,预处理 4 0min后缺氧复氧。与复氧后测定细胞存活率 ,培养液中乳酸脱氢酶、肌酸激酶含量 ,细胞内丙二醛及游离Ca2 + 的变化。结果 与正常组相比 ,Gly处理组和正常组各指标无明显差别 ;与正常组相比 ,单纯缺氧 /复氧组乳酸脱氢酶、肌酸激酶、细胞内丙二醛水平显著升高 (P<0 0 1) ,与正常组相比 ,细胞存活率显著降低 (P <0 0 1)及发生明显钙超载 (P <0 0 1) ;1mmol/LSNAP预处理组明显减轻上述变化 (P <0 0 1) ;而与NO预处理组相比 ,Gly +SNAP预处理组取消了NO组上述保护作用 (P <0 0 1)。结论 KATP通道参与介
Objective To investigate the protective effect of adenosine triphosphate-sensitive potassium channel (KATP) on the injury of hypoxia / reoxygenation cardiomyocytes by nitric oxide (NO). Methods The model of cell hypoxia / reoxygenation injury was established. The cultured cells were randomly divided into 5 groups: group A, normal control group (cultured for 3 hours), group B, glybenclamide (Gly, Group C, simple hypoxia / reoxygenation group (A / R hypoxia 2h, reoxygenation 1h); group D, nitric oxide pretreatment group, adding S SNAP was added to make the final concentration of 1mmol / L, pretreated for 40min followed by hypoxia and reoxygenation; E, Gly + SNAP pretreatment group, the final concentration was 10 μmol / LGly. After incubation for 20 min, SNAP was added to a final concentration of 1 mmol / L. After pretreatment for 40 min, hypoxia / reoxygenation was performed. After reoxygenation, the cell viability, the contents of lactate dehydrogenase, creatine kinase, intracellular malondialdehyde and free Ca2 + were measured. Results Compared with the normal group, there was no significant difference between the Gly group and the normal group. Compared with the normal group, the levels of lactate dehydrogenase, creatine kinase and intracellular malondialdehyde in hypoxia / reoxygenation group were significantly increased (P <0.01). Compared with the normal group, the cell viability was significantly decreased (P <0.01) and the calcium overload was significantly increased (P <0.01). The pretreatment with 1 mmol / L LSNAP significantly reduced the above changes P <0.01). Compared with NO pretreatment group, Gly + SNAP pretreatment group canceled the above protective effect of NO group (P <0.01). Conclusions KATP channels involved in mediation