Effect of alteration of caveolin-1 expression on doxorubicin-induced apoptosis in H9c2 cardiac cells.

摘要: Doxorubicin is an anthracycline antibiotic widely used in cancer treatment. Although its antitumor efficacy appears to be dose dependent, clinical use greatly restricted by the development of cardiotoxicity associated with apoptosis. caveolin-1, major structural protein caveolae, can positively or negatively regulate apoptosis depending on stimulus cell types, contribution caveolin-1 doxorubicin-induced remains unknown. This study was performed identify regulatory role H9c2 cardiac cells using a genetic approach. Caveolin-1 knockdown short hairpin (sh) RNA adenovirus, but not overexpression wild-type resulted marked inhibition caspase-3 cleavage. However, tended protect against decrease viability, it did significantly reverse death induced doxorubicin. stimulated phosphorylation p38 and extracellular signal regulated kinase (ERK). Doxorubicin-induced cleavage inhibited U0126, MEK inhibitor SB203580, inhibitor. markedly p-38 ERK-mediated p-53 cells. Our results suggest that reduced expression plays anti-apoptotic insufficient prevent such