OBJECTIVETo study the protective effect of alcohol extract of Plumula Nelumbini (AEPN) on carbon tetrachloride (CCl4) induced hepatic fibrosis rats and to explore its possible mechanism.

METHODSTotally 32 male SD rats were randomly divided into four groups, i.e., the normal control group, the model group, the high dose AEPN group, and the low dose AEPN group, 8 in each group. 1,000 mg/kg AEPN was given to rats in the high dose AEPN group by gastrogavage at 10 mL/kg, once daily, while 500 mg/kg AEPN was given to rats in the low dose AEPN group by gastrogavage at 10 mL/kg, once daily. Hepatic fibrosis was induced by intraperitoneal injection of CCl4. Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and albumin (ALB) were examined using automatic biochemical analyzer. Activities of superoxide dismutase (SOD), contents of malondialdehyde (MDA) and hydroxyproline (Hyp) in the hepatic tissue were determined using colorimetry. The degree of liver fibrosis was observed by HE staining and Masson staining. The expression of α-smooth muscle actin (α-SMA) was detected using immunohistochemistry.

RESULTS(1) Compared with the normal control group, serum levels of ALT and AST obviously increased and the serum ALB level obviously decreased in the model group (all P < 0.05). After treated by AEPN, serum levels of ALT and AST were lowered. and the serum ALB level was higher (all P < 0.05). (2) Compared with the normal control group, collagen deposition was obviously seen in rats' livers of the model group, and pseudolobule had formed; inflammatory activities and fibrosis degrees were serious; contents of Hyp also increased (P < 0.05).After treated by AEPN, collagen deposition was obviously reduced with no obvious pseudolobule; inflammatory activities and fibrosis degrees were alleviated; contents of Hyp were also lowered (P < 0.05). (3) Compared with the normal control group, contents of MDA in the liver tissue obviously increased, while activities of SOD obviously decreased (P < 0.05) in the model group. After treated by AEPN, contents of MDA in the liver tissue decreased and the serum SOD level significantly increased (all P < 0.05). (4) Compared with the normal control group, the expression of α-SMA was obviously elevated in the model group (P < 0.05). After treated by AEPN, its expression was obviously lowered (P < 0.05).

CONCLUSIONSAEPN could fight against CCl4 induced liver fibrosis in rats. Fighting against lipid peroxidation and inhibi- ting activation and proliferation of hepatic stellate cells might be possibly main mechanism.