Alcohol abuse is one of the major causes of liver fibrosis, which shows a sharply increasing trend worldwide, yet effective therapeutic options for advanced alcohol fibrosis are limited. Recently we investigated the effect of anti-fibrosis by isoorientin-2″-O-α-L-arabinopyranosyl (IOA) isolated from Gypsophila elegans. During the experiment, the model group received alcohol only, and treatment groups received the corresponding drugs plus alcohol respectively, while the normal control group received an equal volume of saline. Analysis at the end of 24-week experiments showed that IOA could significantly improve the liver function, as indicated by decreasing levels of alanine transaminase, aspartate transaminase, alkaline phosphatase, γ-glutamyltransferase, interleukin-6 and tumor necrosis factor-α. Moreover, IOA could effectively inhibit collagen deposition and reduce the pathological tissue damage. Research on mechanism showed that IOA was able to markedly reduce lipid peroxidation, recruit the anti-oxidative defense system, and induce HSC apoptosis by down-regulating bcl-2 mRNA, as well as inhibit the expression of α-smooth muscle actin and transforming growth factor β1 proteins. In short, our results showed that IOA is effective in attenuating hepatic injury and fibrosis in the alcohol-induced rat model, which should be developed as a new drug to treat liver fibrosis and even cirrhosis.
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