苯那普利对乳鼠缺氧复氧心肌细胞肿瘤坏死因子的影响

Influence of benazepril on TNF-α in rats heart cells after hypoxia and reoxygenation

目的观察苯那普利对乳鼠心肌细胞缺氧复氧损伤时肿瘤坏死因子(TNF-α)的影响和可能机制。方法采用纯化的乳鼠心肌细胞复制缺血再灌注模型。实验分5组:正常对照组、单纯缺氧复氧组(HR)、缺氧复氧+苯那普利低剂量组(1×10-7mol/L)、缺氧复氧+苯那普利中剂量组(1×10-6mol/L)和缺氧复氧+苯那普利高剂量组(1×10-5mol/L)。细胞缺氧1h复氧2h后取细胞培养液测定TNF-α及乳酸脱氢酶(LDH)的活性,取细胞测定超氧化物歧化酶(SOD)活性和丙二醛(MDA)含量。结果单纯缺氧复氧组与对照组比较,TNF-α(40.32±5.54和5.43±3.32,P<0.05)、LDH(27.83±2.71和8.0±1.41,P<0.01)和MDA(0.757±0.036和0.131±0.029,P<0.01)含量增高,SOD活性明显降低(对照组为36.13±1.43,其他各组为13.20±1.10、8.87±1.43、21.84±1.31、24.34±1.07,分别为P<0.01和P<0.05);各组苯那普利均减弱TNF-α的表达,减少MDA的生成和LDH的释放,明显提高SOD活性,并呈剂量依赖趋势。结论苯那普利可抑制乳鼠缺氧复氧心肌细胞过度分泌TNF-α,具有明显的抗缺氧复氧损伤、保护心肌的作用。

Objctive To investigate effects of benazepril on cardiomyoeytes TNF-α during hepexia-reoxygenation injury and relation between dose and infect. Methods Cardiomyocytes were made into hepexia-reoxygenation models. Tests were devidod 5 groups： control group, hepexia-reoxygenation group, 3 groups benapril （1 × 10^-7 mol/L, 1×10^-4 mol/L, 1×10^-5 mol/L）. Samples were observed at the time of 1 h after hypersia and 2 h after reoxygenation. Index include Content of TNF-α, LDH, malordaldehvde（MDA）, and super-oxide dismutes （SOD）. Results In＇HR group, express of TNF-α and content of MDA increase, but SOD activity decrease compare with control group. Benazepril alleviate express of TNF-α, reduce content of MDA and LDH, and enhance SOD activity. Conclusion Benazepril can bate exress of TNF-α in hepoxia-reoxygenation of eardiomyocytes, and have distinct protective effects on eardiomyoeytes.