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Protective effect of baicalein on cardiomyoblasts H9C2 against damage induced by oxidative stress
Author(s) -
You YaChing,
Ou HsiuChung
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.785.6
Subject(s) - baicalein , oxidative stress , scutellaria baicalensis , reactive oxygen species , apoptosis , viability assay , chemistry , pharmacology , mitochondrion , microbiology and biotechnology , downregulation and upregulation , biochemistry , biology , medicine , pathology , alternative medicine , traditional chinese medicine , gene
Oxidative stress plays an important role in many cardiovascular diseases. In this study, the effects of baicalein, a natural flavonoid isolated from the root of Scutellaria baicalensis G., on hydrogen peroxide (H2O2)‐induced cytotoxicity in cardiomyoblasts H9C2 were investigated. Treatment with H2O2 markedly decreased the viability of H9C2 cells in a dose‐ and time‐dependent manner, accompanied by increased reactive oxygen species (ROS) generation, mitochondrial dysfunction, downregulation of Bcl‐2, upregulation of Bax, and subsequent cell apoptosis. Pretreatment of H9C2 cells with baicalein inhibited H2O2‐induced cell viability loss, intracellular ROS generation. Furthermore, baicalein potentially inhibited H2O2‐induced cell apoptosis characterized with the DNA fragment. Consistently, the mitochondrial pathway involving the mitochondrial dysfunction associated with cell apoptosis including membrane potential loss, the release of cytochrome c, the disturbance of Bcl‐2 family proteins induced by H2O2 were also abrogated in the presence of baicalein. Taken together, these results suggest that baicalein can block H2O2‐induced apoptosis by prevention of oxidative stress as well as regulation of Bcl‐2 family members and suppression of mitochondria dysfunction, which might be beneficial for the treatment of oxidative stress‐associated cardiovascular diseases.