rh-BNP对大鼠心肌细胞H9c2缺氧/复氧损伤的保护作用及机制  

Protective effect and mechanism of rh-BNP on hypoxia/reoxygenation injury of H9c2 rat cardiomyocytes

作　　者：谭力力[1] 刘丽敏[1] 张秀春 姜贞宇 彭诚铖 TAN Li-li;LIU Li-min;ZHANG Xiu-chun;JIANG Zhen-yu;PENG Cheng-cheng(Department of Vasculocardiology,the Second Affiliated Hospital of Shenyang Medical College,Shenyang 110002,Liaoning,CHINA)

机构地区：[1]沈阳医学院附属第二医院心血管内科,辽宁沈阳110002

出　　处：《海南医学》2018年第21期2964-2967,共4页Hainan Medical Journal

基　　金：辽宁省自然科学基金(编号:2016010726-301);辽宁省沈阳市科技局课题(编号:F16-206-9-17)

摘　　要：目的探讨重组人脑钠肽(rh-BNP)对大鼠H9c2心肌细胞缺氧/复氧损伤后氧化应激的影响及机制。方法将培养的大鼠H9c2细胞分为对照组、H/R模型组和rh-BNP处理组。采用MTT法检测处理后各组细胞的活力;试剂盒测定细胞中丙二醛(MDA)的含量及超氧化物歧化酶(SOD)的活性;Real-time PCR检测核因子NF-E2相关因子(Nrf2)和血红素氧合酶-1 (HO-1)的相对表达量。结果 H/R模型组的相对细胞活力为(30.75±4.74)%,低于对照组的100%;rh-BNP处理组的细胞活力为(58.31±6.53)%,高于H/R模型组的(30.75±4.74)%,差异均具有统计学意义(P<0.05)。H/R模型组细胞中MDA含量为(3.92±0.27),明显高于对照组的(1.43±0.12);SOD活性为(114.72±14.80),明显低于对照组的(236.99±20.45);而rh-BNP处理组细胞MDA含量为(2.23±0.34),明显低于H/R模型组的(3.92±0.27);SOD活性为(153.17±14.64),明显高于H/R模型组的(114.72±14.80),差异均具有统计学意义(P<0.05)。H/R模型组Nrf2和HO-1的相对表达量分别为(0.58±0.04)、(0.44±0.04),均低于对照组,rh-BNP处理组的Nrf2和HO-1的相对表达量分别为(0.81±0.02)和(0.76±0.02),明显高于H/R模型组,差异均具有统计学意义(P<0.05)。结论 rh-BNP对H9c2细胞的缺氧/复氧损伤具有一定的保护作用,能够降低氧化应激水平,Nrf2/HO-1通路可能参与了对这一过程的调控。Objective To investigate the effects and mechanism of recombinant human brain natriuretic peptide （rh-BNP） on oxidative stress induced by hypoxia/reoxygenation in H9c2 rat cardiomyocytes. Methods The cultured H9c2 cells were divided into control group, H/R model group and rh-BNP treatment group. The viability of treated cells after treatment was detected by MTT assay. The kit was used to detect the content of malondialdehyde （MDA） and the activity of superoxide dismutase （SOD）. Real-time PCR was used to detect the relative expression of nuclear factor erythroid 2-related factor2 （Nrf2） and hemeoxygenase-1 （HO-1）. Results The relative cell viability in the H/R model group （30.75±4.74）% was lower than 100% in the control group, and the cell viability in the rh-BNP group （58.31±6.53）%） was higher than （30.75±4.74）% in the H/R group, with statistically significant difference （P〈0.05）. The MDA content in H/R model group was （3.92±0.27）, which was higher than （1.43±0.12） in the control group, but the activity of SOD in H/R group was （114.72±14.80）, which was lower than （236.99±20.45） in the control group. The MDA content in rh-BNP treatment group was （2.23±0.34）, which was lower than （3.92±0.27） in H/R group, and the activity of SOD was （153.17±14.64）, which was higher than （114.72±14.80） in H/R group （P〈0.05）. The relative expression of Nrf2 and HO-1 were （0.58±0.04）, （0.44±0.04） in H/R model group, which were lower than those in the control group. The relative expression of Nrf2 and HO-1 were （0.81±0.02）, （0.76±0.02） in the rh-BNP group, which were higher than those in H/R model group, with statistically significant difference （P〈0.05）. Conclusion Rh-BNP has a protective effect on hypoxia/ reoxygenation injury of H9c2 cells, and can reduce the level of oxidative stress. Nrf2/HO-1 pathway may be involved in the regulation of this process.

关 键 词：重组人脑钠肽 心肌细胞 氧化应激 核因子NF-E2相关因子 血红素氧合酶-1 

分 类 号：R-332[医药卫生]