Hepatoprotective effect of Evodia officinalis Dode on carbon tetrachloride induced liver injury in rats

Abstract

Objective To investigate the protective effect of ethanol extract from Evodia officinalis Dode(EEEO) in a rat model of acute hepatic necrosis induced by carbon tetrachloride (CCl4).Methods Wistar rats were divided into four groups (control,CCl4,EEEO + CCl4,and Silmyarin + CCl4),the four groups were given intragastrically with normal saline,EEEO for 5 d,respectively.In the last one day,these groups except for control group were injected peritoneally with CCl4.Serum levels of alanine aminotransferase (ALT),aspartate aminotransferase (AST),alkaline phosphatase (ALP) were detected by automatic biochemistry analyzer.Pathological changes of hepatic tissues were assessed by hematoxylin-eosine (HE) staining.The levels of superoxide dismutase (SOD),catalase (CAT) and malondialdehyde (MDA) in liver homogenate were analyzed using xanthinoxidase and thio-barbituric acid,respectively.Results Compared the ALT [(345.4 ±51.6)U/ml] and AST [(621.7 ± 143.5) U/ml)] of CCl4 group with ALT [(41.1 ± 2.2) U/ml] and AST [(85.2 ± 22.2) U/ml] of control group,the serum levels of ALT and AST in the CCl4 group were increased significantly (P ＜ 0.05).HE staining of liver tissue,the degeneration and necrosis were implicated to the whole hepatic lobules in the CCl4 group.In EEEO + CCl4 group,compared the ALT [(308.1 ± 44.6) U/ml] and AST [(546.4 ± 131.6) U/ml] of low dose EEEO + CCl4 group with the ALT [(210.6 ±34.5) U/ml] and AST [(379.3 ± 112.3) U/ml] of high dose EEEO +CCl4 group the serum levels of ALT and AST were decreased significantly in low dose EEEO + CCl4 group (P ＜0.05).The denaturation and necrosis of hepatic lobules,the level of SOD,CAT were increased and MDA decreased (P ＜ 0.05) inendochylema.Concluslons EEEO can significantly relieve the CCl4-induced hepatonecrosis.The role may be related to anti-lipid peroxidation. Key words: EVODIA RUTAECARPA; Plant extracts/pharmacology; Ethanol; Hepatitis, toxic/ZHONG YAO LIAO FA; Carbon tetrachloride poisoning; Acute disease