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      Catalpol inhibits apoptosis in hydrogen peroxide-induced PC12 cells by preventing cytochrome c release and inactivating of caspase cascade.

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      Animals, Apoptosis, drug effects, genetics, Caspases, metabolism, Cytochromes c, Drugs, Chinese Herbal, pharmacology, Gene Expression Regulation, Genes, bcl-2, Glucosides, Hydrogen Peroxide, Iridoid Glucosides, Iridoids, PC12 Cells, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-bcl-2, Rats, bcl-2-Associated X Protein

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          Abstract

          In the present study, using a rat pheochromocytoma (PC12) cell line, the effect of catalpol on H2O2-induced apoptosis was studied. The apoptosis in H2O2-induced PC12 cells was accompanied by down-regulation of Bcl-2, up-regulation of Bax, the release of mitochondrial cytochrome c to cytosol and sequential activation of caspase-1 and caspase-3 then leading to cleavage of poly-ADP-ribose polymerase (PARP). Catalpol not only suppressed the down-regulation of Bcl-2, up-regulation of Bax and the release of mitochondrial cytochrome c to cytosol, but also attenuated caspase-3 activation, PARP cleavage, and eventually protected against H2O2-induced apoptosis. Taken together, these results suggest that treatment of PC12 cells with catalpol can block H2O2-induced apoptosis by the regulation of Bcl-2 family members, as well as suppression of cytochrome c release and caspase cascade activation.

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