Abstract
Babao Dan (BBD), a traditional Chinese medicine, has been widely used as a complementary and alternative medicine to treat chronic liver diseases. In this study, we aimed to observe the protective effect of BBD on rat hepatic fibrosis induced by diethylnitrosamine (DEN) and explore it possible mechanism. BBD was administrated while DEN was given. After eight weeks, values of serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) indicated that BBD significantly protected liver from damaging by DEN and had no obvious side effect on normal rat livers. Meanwhile, BBD attenuated hepatic inflammation and fibrosis in DEN-induced rat livers through histopathological examination and hepatic hydroxyproline content. Furthermore, we found that BBD inhibited hepatic stellate cells activation and proliferation without altering the concentration of lipopolysaccharide (LPS) in portal vein. In vitro study, serum from BBD treated rats (BBD-serum) could also significantly suppress LPS-induced HSCs activation through TLR4/NF-κB pathway. In addition, BBD-serum also inhibited the proliferation of HSCs by regulating TLR4/ERK pathway. Our study demonstrated that BBD may provide a new therapy strategy of hepatic injury and hepatic fibrosis.
Highlights
Hepatic fibrosis, characterized by excessive accumulation of extracellular matrix (ECM) proteins, occurs in most types of chronic liver diseases [1,2,3]
We demonstrated that BBD can ameliorate liver injury and fibrosis in rat hepatic fibrosis model induced by diethylnitrosamine (DEN), and have no obvious side effect in normal rat livers
We showed the therapeutic function of Babao Dan (BBD) in DEN-induced rat hepatic fibrosis and explored the possible mechanisms
Summary
Hepatic fibrosis, characterized by excessive accumulation of extracellular matrix (ECM) proteins, occurs in most types of chronic liver diseases [1,2,3]. Focusing on events that lead to the primarily accumulation of ECM help to develop new therapeutic targets to attenuate hepatic fibrosis. Quiescent hepatic stellate cells (HSCs) are located in Disse space and characterized by storage of retinoid. Activated HSCs are demonstrated as predominant cell produced ECM to participate in hepatic fibrosis [7, 8]. Activated HSCs regulate the recruitment of inflammatory cells via secretion of chemotactic factors, such as MCP-1. Inhibition of the HSCs activation and proliferation may be an attractive method to anti-fibrotic therapy [9]
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