Published online Nov 14, 2014. doi: 10.3748/wjg.v20.i42.15703
Revised: May 14, 2014
Accepted: June 21, 2014
Published online: November 14, 2014
Processing time: 228 Days and 21.4 Hours
AIM: To evaluate protective effects of Chunggan extract (CGX), a traditional herbal formula, under 4 wk of alcohol consumption-induced liver injury.
METHODS: Male Sprague-Dawley Rats were orally administered 30% ethanol daily for 4 wk with or without CGX. The pharmaceutical properties were assessed through liver enzymes, histopathology, fibrogenic cytokines, and alcohol metabolism in hepatic tissues as well as by in vitro experiment using HSC-T6 cells.
RESULTS: Four weeks of alcohol consumption notably increased liver enzymes and malondialdehyde levels in serum and hepatic tissue. CGX not only prevented the collagen deposition determined by histopathology and hydroxyproline content, but also normalized transforming growth factor-beta, platelet-derived growth factor-beta and connective tissue growth factor at the gene expression and protein levels in liver tissue. Moreover, CGX treatment also significantly normalized the abnormal changes in gene expression profiles of extracellular matrix proteins, matrix metalloproteinase and their inhibitors, alcohol metabolism, and inflammatory reactions. In the acetaldehyde-stimulated HSC-T6 cells, CGX considerably inhibited collagen production and normalized fibrogenic cytokines in both gene expression and protein levels.
CONCLUSION: The present study evidenced that CGX has hepatoprotective properties via modulation of fibrogenic cytokines and alcohol metabolism in alcoholic liver injury.
Core tip: We observed that the protective effect of Chunggan extract (CGX) on alcohol induced rat model of hepatic injury. In this study, 4 wk of alcohol consumptions markedly induced hepatic injury. Treatment with CGX significantly reverses and ameliorates pro-fibrogenic cytokines including transforming growth factor-β, platelet-derived growth factor-BB, and connective tissue growth factor. We also revealed the significant effects of alcohol metabolism related molecules by CGX treatment. The pharmacological actions were supported by in vitro assay that acetaldehyde stimulated HSC-T6 cell activation was normalized by CGX. Collectively our results suggest that CGX will be applicable to treat patients with alcoholic liver injury through amelioration of fibrotic changes and alcohol metabolisms.