Protective effect of calceolarioside on adriamycin-induced cardiomyocyte toxicity

被引:26
|
作者
Kim, Do-Sung
Kim, Hyung-Ryong
Woo, Eun-Rhan
Kwon, Dae-Young
Kim, Myung-Sunny
Chae, Soo-Wan [1 ]
Chae, Han-Jung
机构
[1] Chonbuk Univ, Sch Med, Dept Pharmacol, Chonbuk 560180, South Korea
[2] Chonbuk Univ, Sch Med, Cardiovasc Res Inst, Chonbuk 560180, South Korea
[3] Wonkwang Univ, Sch Dent, Dept Dent Pharmacol, Chonbuk 570749, South Korea
[4] Wonkwang Univ, Sch Dent, Wonkwang Biomat Implant Res Inst, Chonbuk 570749, South Korea
[5] Chosun Univ, Coll Pharm, Kwangju 501759, South Korea
[6] Chosun Univ, Res Ctr Proteineous Mat, Kwangju 501759, South Korea
[7] Korea Food Res Inst, Kyonggi Do 463746, South Korea
关键词
calceolarioside; adriamycin; apoptosis; reactive oxygen species;
D O I
10.1016/j.ejphar.2006.04.045
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Adriamycin is a potent antitumor drug that is known to cause severe cardiotoxicity. This study examined the protective effect of calceolarioside on adriamycin-induced cardiomyocyte toxicity. Calceolarioside significantly inhibited the adriamycin induced cell death and caspase-3 activation, which may be explained by the increase in Bcl-2 expression and the inhibition of Bax expression. Calceolarioside increased the expression of the antioxidant molecules and decreased the level of intracellular reactive oxygen species. Catalase, glutathione, N-acetylcysteine, Mannitol and Mn-TBAP (manganese (III) tetrakis-(4-benzoic acid) porphyrin) significantly inhibited the H9c2 cell death induced by adriamycin. Calceolarioside significantly inhibited H9c2 cell death, and was more effective than that observed with the other antioxidants, including probucol, ascorbic acid, and alpha-tocopherol. Overall, these results suggest that calceolarioside can inhibit adriamycin-induced apoptosis in H9c2 cardiomyocyte by inhibiting the generation of reactive oxygen species. Calceolarioside may be a potential candidate agent that inhibits cardiomyocyte-toxicity in adriamycin-exposed patients. (c) 2006 Elsevier B.V All rights reserved.
引用
收藏
页码:24 / 32
页数:9
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