BACKGROUND: Hepatic fibrosis is a chronic progressive disorder with a poor prognosis for which no definitive treatment exists. S-allylcysteine (SAC), an ingredient of aged garlic extract, is known to have antioxidant and hepatoprotective effects. The aim of this study was to investigate the antifibrotic effects of SAC in the liver. METHODS: Hepatic fibrosis was induced in male Wistar rats by porcine serum (PS) intraperitoneal injection. SAC (0.15% of basal diet) or N-acetylcysteine (NAC, 0.45% of basal diet) was orally administered for 12 weeks. Liver damage was assessed by the levels of plasma alanine aminotransferase (ALT), hepatic lipid peroxides (LPO), and hepatic total thiols 12 weeks after first PS injection. Area of fibrosis was examined by Azan-Mallory staining. Hydroxyproline content of liver were assessed as an index of collagen content. Liver was examined for expression of alpha-smooth muscle actin (alpha-SMA) as a marker of hepatic stellate cell (HSC) activation. RESULTS: There were no significant differences in levels of plasma ALT, hepatic LPO, or hepatic total thiols among the groups. PS significantly increased area of fibrosis and hydroxyproline content in the liver. SAC and NAC each markedly attenuated the development ofhepatic fibrosis. SAC and NAC markedly suppressed the PS-induced increase in alpha-SMA expressions. CONCLUSIONS: Oral administration of SAC reduced PS-induced hepatic fibrosis in rats via inhibition of HSC activation. SAC could provide a new therapeutic strategy for hepatic fibrosis.
BACKGROUND:Hepatic fibrosis is a chronic progressive disorder with a poor prognosis for which no definitive treatment exists. S-allylcysteine (SAC), an ingredient of aged garlic extract, is known to have antioxidant and hepatoprotective effects. The aim of this study was to investigate the antifibrotic effects of SAC in the liver. METHODS:Hepatic fibrosis was induced in male Wistar rats by porcine serum (PS) intraperitoneal injection. SAC (0.15% of basal diet) or N-acetylcysteine (NAC, 0.45% of basal diet) was orally administered for 12 weeks. Liver damage was assessed by the levels of plasma alanine aminotransferase (ALT), hepatic lipid peroxides (LPO), and hepatic total thiols 12 weeks after first PS injection. Area of fibrosis was examined by Azan-Mallory staining. Hydroxyproline content of liver were assessed as an index of collagen content. Liver was examined for expression of alpha-smooth muscle actin (alpha-SMA) as a marker of hepatic stellate cell (HSC) activation. RESULTS: There were no significant differences in levels of plasma ALT, hepatic LPO, or hepatic total thiols among the groups. PS significantly increased area of fibrosis and hydroxyproline content in the liver. SAC and NAC each markedly attenuated the development ofhepatic fibrosis. SAC and NAC markedly suppressed the PS-induced increase in alpha-SMA expressions. CONCLUSIONS: Oral administration of SAC reduced PS-induced hepatic fibrosis in rats via inhibition of HSC activation. SAC could provide a new therapeutic strategy for hepatic fibrosis.