Abstract
Liver cirrhosis is one of chronic liver diseases with high disability and mortality accompanying fibrosis, hepatocyte damage, and liver dysfunction. In this study, the hepatoprotective and the antifibrotic properties of lesimarin(lecithin - silymarin - Artemisia messerschmitiana Besser(AMB) extract complex at 11:3:6 ratio) on rat hepatic fibrosis induced by thioacetamide (TAA) was investigated. Rats were divided into seven groups: control, lesimarin, TAA, TAA+lesimarin, TAA+lecithin, TAA+silymarin, TAA+AMB. Rats were administered with TAA at a dose of 200 mg/kg body weight intraperitoneally twice a week for three months. Lesimarin, lecithin, silymarin and AMB were administered at a dose of 1.0, 1.0, 0.5, 1.0g/kg body weight orally daily for three months, respectively. TAA administration resulted in hepatic fibrosis, significant decrease in body weight, albumin level and A/G ratio and increase in plasma transaminase, GGT(γ-glutamyltransferase) and ALP(alkaline phosphatase) activities as well as hepatic hydroxyproline content, which were attenuated by lesimarin administration. Lesimarin was found to decrease AST, ALT and GGT, ALP and bilirubin, hydroxyproline levels and increase albumin level and A/G ratio and its effect is more prominent than those of individual constituents. These results suggest this new drug, lesimarin, might be a promising drug to be used for chronic liver diseases.
Highlights
The liver disorders are very frequent and widely distributed in the world
Recent studies have clearly demonstrated that the excessive accumulation of extracellular matrix in liver fibrotic diseases is a dynamic and bidirectional process which is mainly regulated by hepatic stellate cells (HSC) (Abul et al, 2002)
There was a statistically significant reduction of body weight in rats administered with TAA compared to the normal and lesimarin-treated groups
Summary
Among them hepatic fibrosis represents the response of the liver to different chronic insults, and is associated with significant morbidity and mortality. Recent studies have clearly demonstrated that the excessive accumulation of extracellular matrix in liver fibrotic diseases is a dynamic and bidirectional process which is mainly regulated by hepatic stellate cells (HSC) (Abul et al, 2002). Several in vitro studies have shown that the process of HSC activation results from the complex interplay of different factors, such as cytokines, growth factors, oxidative stress and modification of Na+/H+ exchange activity (Aydin et al, 2010). It has been shown to protect the liver against increased oxidative stress caused by alcohol consumption, CCl4 or TAA and accelerate alcohol metabolism (Chen et al, 2012; Chung-His et al, 2012)
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