Protective effects of Lycium ruthenicum Murr. on hydrogen peroxide-induced cellular oxidative stress injury in heart-derived H9c2 cells
10.3969/j.issn.1006-2157.2018.04.007
- VernacularTitle:黑果枸杞对H2O2诱导的H9c2心肌细胞氧化应激损伤的保护作用研究
- Author:
Huijuan SUN
1
;
Ling DONG
;
Jiaxin WANG
;
Meng PAN
;
Yue WU
;
Sen LI
Author Information
1. 北京中医药大学中药学院 北京102488
- Keywords:
Lycium ruthenicum Murr.;
oxidative damage;
apoptosis;
Bcl-2;
Bax
- From:
Journal of Beijing University of Traditional Chinese Medicine
2018;41(4):301-305
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the protective effects of Lycium ruthenicum Murr. (Lrm) on hydrogen peroxide (H2O2)-induced cellular oxidative stress injury in heart-derived H9c2 cells. Methods In this study,H2O2-induced injury in heart-derived H9c2 cells was established as cellular oxidative stress injury model. The H9c2 cells were divided into blank group,model group(H2O2400 μmol/L) and experimental group(Lrm 1.00 g/L +H2O2400 μmol/L). The Lrm group was pretreated with Lrm for 2 h before treated with H2O2for 6 h. Cellular morphology of all groups was observed. Cell viability(MTT assay),apoptosis rate (TUNEL assay),Bcl-2 and Bcl-2 relating x gene protein (Bax) expression were evaluated (Western Blotting). Results Compared with the blank group, abnormal cellular morphology, decreased cell activity,and increased apoptosis were observed in the model group(P<0.05). Anti-apoptotic Bcl-2 gene was less expressed while pro-apoptotic Bax protein level was increased. Compared with the model group, cellular morphology and activity was greatly improved in the experimental group with reduced apoptosis rate (P <0.05). The increased expression of Bcl-2 and reduction of Bax were also significantly different. Conclusion Our findings suggest that Lrm tended to improve the H9c2 myocardial cellular morphology, enhance cell activity and reduce apoptosis rate. Its mechanism of action in reducing oxidative stress injury may be related to the up-regulation of Bcl-2 as well as down-regulation of Bax protein expression.