ABSTRACT
This study was aimed to observe the protective effect of extract from Rhizoma A nemones Raddeanae (RAR) on hepatic fibrosis induced by porcine serum in rats. A total of 68 SD rats were randomly divided into 5 groups, which were the normal group, model group, RAR group, extraction of RAR (EXRAR) group, Fu-Zheng Hua-Y u(FZHY) group. Each rat was intraperitoneally injected with 0.5~0.6 ml of porcine serum twice a week for 15 suc-cessive weeks to establish liver fibrosis model. Intragastric administration was given after the model was successfully established. The FZHY group was given FZHY capsule (0.525 g·kg-1). The RAR group was given RAR decoction (0.7 g·kg-1). The EXRAR group was given EXRAR (0.071 g·kg-1). The model group and normal group were given e-qual amount of physiological saline. The medication was given once a day. And the treatment course was 8 weeks. At the end of the 23th week, rats were sacrificed. Contents of SOD and MDA in blood serum were assayed. The protein expressions of α-SMA and TGF-β1 in liver tissues were detected by SABC. The results showed that compared with the model group, content of MDA decreased in the EXRAR group, RAR group and FZHY group (P<0.05), and content of SOD increased obviously (P<0.05). In the model group, expression of α-SMA and TGF-β1 increased, with dark brown dyeing and diffusion area. Expression area and strength of the FZHY group, RAR group, and EXRAR group were ob-viously weak with tasteless interval dyeing and no formation of typical pseudolobule in comparison with the model group. The color rendering index showed that compared with the model group, the protein expression of α-SMA and TGF-β1 decreased obviously in liver tissues of the FZHY group, EXRAR group, and RAR group (P< 0.05). It was concluded that RAR and its extract had a good antifibrosis effect. And the EXRAR had basically the same antifibrosis effect as RAR. It was assumed that the possible mechanism was related with the inhibiting of hepatic stellate cell (HSC) activation and the expression of TGF-β1 as well as the resisting of lipid peroxidation.