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Daya Ram Parajuli,Yu-Zhe Zhao,Hao Jin,Jin Hua Chi,Si Yuan Li,김윤철,손동환,이성희 대한약학회 2015 Archives of Pharmacal Research Vol.38 No.4
We previously reported the in vitro and in vivohepatoprotective and anti-fibrotic effects of PF2401-SF, astandardized fraction of Salvia miltiorrhiza, against acuteand subacute liver injury. The aim of this study was toinvestigate the effect of PF2401-SF on liver fibrosisinduced by thioacetamide (TAA), a chronic liver injurymodel (12 weeks) that closely resembles fibrosis and cirrhosisin humans. Hepatoprotective activity was indicatedby low serum levels of the markers aspartate aminotransferase and alanine amino transferase .In addition,compared to the TAA-group livers, the PF2401-SF-treatedliver tissues showed no fibrous tissue deposition in theportal areas, hepatocyte morphology more closely resemblingnormal tissue morphology, and significantly reducedcollagen deposition. Furthermore, downregulation of collagen1(a) and tissue inhibitor of metalloproteinase(TIMP)1 protein and mRNA expression also supportsPF2401-SF’s anti-fibrotic effect. We also observed reducedexpression of a-smooth muscle actin (a-SMA), an importantmarker of hepatic stellate cells (HSCs) activation. From these results, we conclude that PF2401-SF’s antifibroticmechanism in the TAA model involves reducedHSC activation, and may be mediated by downregulationof central markers of fibrosis, including collagen 1(a),TIMP1, and a-SMA.
Apoptotic Effect of Propyl Gallate in Activated Rat Hepatic Stellate Cells
Xian-Hua Che,손동환,Wen-Yi Jiang,Daya Ram Parajuli,Yu-Zhe Zhao,이성희 대한약학회 2012 Archives of Pharmacal Research Vol.35 No.12
Hepatic stellate cells (HSCs) play a central role in liver fibrosis. Inhibition of HSC growth and induction of apoptosis have been proposed as therapeutic strategies for the treatment and prevention of liver fibrosis. Propyl gallate (PG) is an antioxidant widely used in processed foods, cosmetics and medicinal preparations. However, the anti-fibrotic effect of PG in liver injury is unclear. In this study, we investigated whether PG could induce apoptosis in activated HSCs. Treatment of activated HSCs with PG inhibited cell viability in a dose- and time-dependent manner. PG induced apoptosis as demonstrated by morphological changes, poly(ADP-ribose) polymerase (PARP) cleavage, caspase-3 cleavage, increased Bad expression, and decreased Bcl-2 protein expression. Through stimulation of the activation of c-Jun NH2-terminal protein kinase (JNK) and p38 mitogen-activated protein kinases (MAPK) by PG treatment, we demonstrated that JNK and p38 MPAK are not involved in PG-induced apoptosis using their specific inhibitors. Taken together, these findings indicate that PG induces apoptosis in activated HSCs. The potential anti-fibrotic effect of PG warrants further evaluation.