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Protection of epidermal growth factor against clivorine‐induced mitochondrial‐mediated apoptosis in hepatocytes
Pyrrolizidine alkaloids (PAs) are well‐known natural hepatotoxins. In this study, we investigated the protection of epidermal growth factor (EGF) against the hepatotoxicity of clivorine, which is an otonecine‐type PA from traditional Chinese medicine Ligularia hodgsonii Hook. Cell viability assay and cell morphology observation showed that EGF (1 ng/mL) reversed clivorine‐induced cytotoxicity on human normal liver L‐02 cells. EGF (1 ng/mL) also inhibited clivorine‐induced DNA fragmentation and caspase‐3 cleavage. Our previous study has showed that antiapoptotic Bcl‐xL degradation and mitochondrial‐mediated apoptosis was involved in clivorine‐induced hepatotoxicity. In this study, we found that EGF (1 ng/mL) inhibited clivorine‐induced antiapoptotic Bcl‐xL protein decrease, caspase‐9 activation, and release of cytosolic cytochrome C. We further investigated the effects of vascular epidermal growth factor, basic fibroblast growth factor, and insulin‐like growth factor‐1 on clivorine‐induced cytotoxicity, and there is no significant protection observed. Our results suggest that EGF exerts its protective effects against clivorine‐induced hepatotoxicity probably by modulating mitochondrial‐mediated apoptotic signal pathway. © 2009 Wiley Periodicals, Inc. Environ Toxicol, 2010.
Protection of epidermal growth factor against clivorine‐induced mitochondrial‐mediated apoptosis in hepatocytes
Pyrrolizidine alkaloids (PAs) are well‐known natural hepatotoxins. In this study, we investigated the protection of epidermal growth factor (EGF) against the hepatotoxicity of clivorine, which is an otonecine‐type PA from traditional Chinese medicine Ligularia hodgsonii Hook. Cell viability assay and cell morphology observation showed that EGF (1 ng/mL) reversed clivorine‐induced cytotoxicity on human normal liver L‐02 cells. EGF (1 ng/mL) also inhibited clivorine‐induced DNA fragmentation and caspase‐3 cleavage. Our previous study has showed that antiapoptotic Bcl‐xL degradation and mitochondrial‐mediated apoptosis was involved in clivorine‐induced hepatotoxicity. In this study, we found that EGF (1 ng/mL) inhibited clivorine‐induced antiapoptotic Bcl‐xL protein decrease, caspase‐9 activation, and release of cytosolic cytochrome C. We further investigated the effects of vascular epidermal growth factor, basic fibroblast growth factor, and insulin‐like growth factor‐1 on clivorine‐induced cytotoxicity, and there is no significant protection observed. Our results suggest that EGF exerts its protective effects against clivorine‐induced hepatotoxicity probably by modulating mitochondrial‐mediated apoptotic signal pathway. © 2009 Wiley Periodicals, Inc. Environ Toxicol, 2010.
Protection of epidermal growth factor against clivorine‐induced mitochondrial‐mediated apoptosis in hepatocytes
Ji, Lili (author) / Liu, Tianyu (author) / Wang, Zhengtao (author)
Environmental Toxicology ; 25 ; 304-309
2010-06-01
6 pages
Article (Journal)
Electronic Resource
English
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