Protective effect of quercetin on L-02 cells by inhibiting DNA damage of INH-induced mitochondrial oxidative stress
10.3969/j.issn.1000-4718.2015.02.021
- VernacularTitle:槲皮素抑制异烟肼诱导的 L-02细胞线粒体氧化应激性 DNA 损伤
- Author:
Chunfeng LU
;
Shuqiu WANG
;
Tingyu CHEN
;
Mingyuan ZHANG
;
Shuxiang WANG
;
Jianjie WANG
;
Qing YUAN
- Publication Type:Journal Article
- Keywords:
Quercetin;
Isoniazid;
Mitochondrial oxidative damage;
L-02 cells;
DNA damage
- From:
Chinese Journal of Pathophysiology
2015;(2):308-312
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate the role of reactive oxygen species ( ROS)-mediated mitochondrial oxidative injury in isonicotinyl hydrazide ( INH)-induced DNA damage and the protective effect of quercetin on L-02 cells.ME-THODS:The injury model of hepatocyte L-02cells in vitro induced by INH was established .The cells were divided into control group, INH group, low-dose quercetin group and high-dose quercetin group.The DNA damage of L-02 cells was evaluated by the comet test .The mitochondrion was prepared , and the level of mitochondrial ROS and the value of mitochondrial membrane potential (ΔΨm ) were detected by fluorescent probes DCFH-DA and rhodamine 123.The content of MDA was measured by TBA method .The activity of SOD was assessed with the xanthine oxidase method .The protein expression of Bcl-2 and Bax was determined by Western blotting , and the value of Bax/Bcl-2 was calculated .RESULTS:INH induced obvious DNA damage , increased the level of mitochondrial ROS , the content of MDA and the value of Bax/Bcl-2, and markedly reduced the value of ΔΨm and the activity of SOD in the L-02 cells.Quercetin attenuated DNA dam-age, reduced the level of mitochondrial ROS , elevated the value of ΔΨm , declined the content of MDA , increased the ac-tivity of SOD and decreased the value of Bax/Bcl-2 in the L-02 cells.CONCLUSION:INH induces DNA damage in L-02 cells by generation of mitochondrial oxidative stress .Quercetin has a protective effect on L-02 cells to attenuate the INH-in-duced DNA damage by inhibiting ROS-mediated mitochondrial oxidative damage .
