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作 者:黄靓[1,2] 王汉群[2] 张弛[1] 高勇强[2] 向琼[2] 王平平[1] 尹卫东[1]
机构地区:[1]南华大学心血管疾病研究所,湖南衡阳421001 [2]南华大学外科学总论教研室,湖南衡阳421001
出 处:《中国药理学通报》2014年第1期104-108,共5页Chinese Pharmacological Bulletin
基 金:湖南省教育厅资助科研项目(No 11C1093;11C1095)
摘 要:目的研究新型褪黑素受体激动剂Neu-P11对心肌细胞缺氧/复氧损伤的作用及分子机制。方法实验分为对照组、缺氧/复氧模型组(H/R组)、H/R+Neu-P11组、H/R+Compound C组、H/R+Neu-P11+Compound C组。构建H9c2心肌细胞缺氧/复氧模型,检测各组心肌细胞凋亡情况,细胞培养液中乳酸脱氢酶(LDH)、肌酸激酶(CK)、SOD活性及MDA含量及心肌细胞AMPK的活性。结果与缺氧/复氧组细胞相比,Neu-P11预处理组细胞凋亡率明显减少,CK、LDH、MDA含量明显下降,SOD活性增加,心肌细胞AMPK活性明显增高,而AMPK特异性抑制剂Compound C可以阻断Neu-P11的保护作用。结论 Neu-P11能够减轻心肌细胞缺氧/复氧损伤,这一保护作用与激活AMPK有关。Ahn To study the protective effects of Neu- P11 on hypoxia/reoxygenation (H/R) injury in H9c2 myocardial cells. Methods The hypoxia/reoxygen (H/R) injury cardiomyocyte model was established in H9c2 myocardial cell strain. The cells were randomly divided into five groups: control group, H/R group, H/R + Neu-P11 group, H/R + Neu-P11 + Compound C group and H/R + Compound C group. Cell apopto-sis of cardiomyocytes was measured by flow cytometry. The activity of lactate dehydrogenase (LDH), creatine kinase (CK), superoxide dismutase (SOD) and the malondialdehyde (MDA) contents were assayed re- spectively in cellular supernate. The activity of AMPK ( AMP-activated protein kinase) was determined, Re- suits Compared with H/R group, H/R + Neu-P11 group decreased apoptotic rate , restrained LDH , CK and AST release evidently, decreased the MDA content and enhanced the SOD activity and phosphorylation level of AMPK ( P 〈 0.05 ) , while significant ameliora- tions in the above indices were seen in H/R + APN group. The activity of LDH and the content of MDA were all increased. Conclusion Neu-P11 exerts pro-tective effect on hypoxia/reoxygenation myocardial cells, which might be related with in H9C2 the activation of AMPK.
关 键 词:Neu—P11 腺苷酸活化蛋白激酶 心肌细胞 缺氧 复 氧损伤 腺苷酸活化蛋白激酶 细胞凋亡 褪黑素
分 类 号:R322.11[医药卫生—人体解剖和组织胚胎学] R329.25[医药卫生—基础医学]
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