Protective effect of ferulic acid on doxorubicin induced cellular injury in H9 c2 myocardial cells
10.3969/j.issn.1001-1978.2014.08.006
- VernacularTitle:阿魏酸预处理对阿霉素诱导H9 c2心肌细胞损伤的保护作用
- Author:
Zhijuan WU
;
Jing YU
;
Ruixing WANG
;
Qiujuan FANG
;
Mojun LIN
- Publication Type:Journal Article
- Keywords:
ferulic acid;
doxorubicin;
cardioprotec-tion;
H9 c2 myocardial cells;
apoptosis;
oxidative stress
- From:
Chinese Pharmacological Bulletin
2014;(8):1059-1065
- CountryChina
- Language:Chinese
-
Abstract:
Aim Tostudytheeffectsofferulicacid (FA) on doxorubicin (DOX) induced cellular injury inH9c2ratmyocardialcells.Methods H9c2cells were treated with 1μmol·L-1 DOX treated for 24 h to establish a myocardial injury model. 10, 20, 40μmol ·L-1 FA was added 2 h before DOX treatment. Cell viability was measured by cell counter kit ( CCK-8 ) . Morphological changes were observed by phase contrast microscope. LDH, CK, MDA, SOD levels were detec-ted by biochemical kits. Intracellular level of reactive oxygen species ( ROS) was examined by DCF-DA stai-ning with flow cytometry. Cellular apoptosis was detec-ted by AO-EB staining and DNA agarose gel electro-phoresis. The expression of caspase-3, Bax, Bcl-2 was evaluatedbyWesternblot.Results Exposureof H9c2 cells to DOX led to decrease in cell viability, in-crease in stress and apoptosis. FA pre-treatment im-proved cell viability in a dose-dependent manner, at-tenuated leakage of LDH and CK, and reversed mor-phological changes induced by DOX. FA suppressed DOX-induced oxidative stress as evidenced by reducing ROS and MDA generation and increasing SOD enzyme activity. FA depressed myocardial apoptosis by down-regulating pro-apoptotic protein caspase-3 and Bax, whereas up-regulating apoptosis inhibitory protein Bcl-2.Conclusions FAhasaprotectiveeffectonDOX-induced injury in H9c2 cells. This protection may re-sult from inhibition of myocardial oxidative stress and apoptosis.
