Effect of neuregulin-1 on cardiomyocyte apoptosis and oxidative damage under hypoxia reoxygenation
10.3969/j.issn.1000-484X.2018.04.005
- VernacularTitle:NRG-1对缺氧复氧心肌细胞凋亡及氧化损伤的影响
- Author:
Jun WANG
1
;
Fen-Ling FAN
;
Song-Lin ZHANG
;
Xing-Ye WANG
;
Jian-Ying XUE
Author Information
1. 西安交通大学第一附属医院结构性心脏病科
- Keywords:
Cardiomyocytes;
Hypoxia reoxygenation;
Apoptosis;
Oxidative damage;
Neuregulin-1
- From:
Chinese Journal of Immunology
2018;34(4):502-507
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To investigate the effect of NRG-1 on cardiomyocyte apoptosis and oxidative damage under hypoxia reox-ygenation.Methods:The myocardial cell HCM was taken as the object of study.The hypoxia reoxygenation of myocardial cell model was established,and NRG-1 at dose of 0.8 mg/L was added before hypoxia.The cell viability was measured by MTT assay and apoptosis was analyzed by flow cytometry.The level of lactate dehydrogenase(LDH) in the supernatant was detected by 2,4-dinitrophe-nylhydrazine colorimetry assay,DCFH-DA method was used to detected ROS level,the level of MDA was measured by thiobarbituric acid method,the level of SOD was detected by xanthine oxidase method,and the protein levels of Akt and p-AktThr308were determined by Western blot.Results:The A values of the myocardial cells after hypoxia reoxygenation were changed from 0.66±0.03 to 0.36±0.04, the rate of apoptosis increased from (4.62±0.97)% to (29.07±3.43)%,the level of ROS increased from 69.29±7.96 to 280.84± 20.52,the levels of LDH and MDA also increased,and the levels of SOD and p-AktThr308/Akt decreased.After NRG-1 treatment,the A values of the cells were from 0.36±0.04 to 0.47±0.05,the rate of apoptosis decreased from (29.07±3.43)% to (19.76±3.41)%, the ROS levels decreased from 280.84±20.52 to 128.23±12.32,the levels of LDH and MDA also decreased,and the levels of SOD and p-Akt/Akt increased.Conclusion: NRG-1partly inhibits cardiomyocyte apoptosis and oxidative damage induced by hypoxia reoxygenation by affecting the protein levels of p-Akt/Akt in the cardiomyocytes.
