ABSTRACT
This article was aimed to study the therapeutic material basis of Xiong-Shao (XS) decoction on hepatic fi-brosis (HF), and screen effective parts from XS decoction for protecting liver, reducing enzyme activity and oxidative damage. Male wistar rats were randomly divided into the normal group, model group, Fu-Zheng Hua-Y u (FZHY) group, XS group, polysaccharide group, total alkaloids group and the total glycosides group. HF rat model was estab-lished with the intraperitoneal injection of DMN. After modeling, FZHY solution (0.105 g·mL-1), XS decoction (1.610 g·mL-1), crude polysaccharides extract of XS decoction (35.420 mg·mL-1), total glycosides extract solution (25.725 mg·mL-1), and total alkaloids extract of XS decoction (0.196 mg·mL-1) were administered to corresponding treatment group by gavage once a day for 4 weeks, respectively. Rats of the normal group and model group were given equiva-lent normal saline by gavage once a day for 4 weeks. After 4-week drug administration, rats were killed to remove the liver. Automatic biochemical analyzer was used in the detection of serum parameters of liver function, including ALT, AST, TIBL and ALB. Serum SOD activity was detected by xanthine oxidase. GSH-PX activity was tested by DTNB reduction. Serum contents of MDA were measured by TBA. Pathological changes of the liver were observed with HE staining and masson staining. The results showed that compared with the model group, there was no signifi-cant differences between the total alkaloids group and the model group, but levels of serum ALT, AST and TBIL of other treatment groups were significantly decreased, and the serum ALB level was significantly elevated (P< 0.05 or P < 0.01). Compared with the model group, levels of serum SOD and GSH-PX of the FZHY group, XS group and total alkaloids group were significantly elevated (P < 0.01), and level of serum MDA was significantly reduced (P <0.05 or P< 0.01). Comparison among the polysaccharides group, total glycosides group, and model group showed no significant differences. It was concluded that crude polysaccharide and total glycosides fractions were effective parts of XS decoction for protecting liver and reducing enzyme activity. And total alkaloids fraction was the effective part for reducing oxidative damage.
ABSTRACT
This study was aimed to study the therapeutic material basis of Xiong-Shao decoction (XSD) on hepatic fi-brosis (HF), and to screen the effective parts from XSD for regulating TGF-β/Smad pathway. Male Wistar rats were randomly divided into the normal group, the model group, the Fu-Zheng Hua-Y u (FZHY) capsule group, the XSD group, the crude polysaccharide group, the total glycosides group, and the total alkaloids group. Rats of the modeling group were intraperitoneally injected with dimethylnitrosamine (DMN) to establish HF model. After modeling, FZHY capsule solution (0.105 g·mL-1), XSD crude polysaccharides extract solution (35.420 mg·mL-1), XSD total glycosides extract solution (25.725 mg·mL-1), and XSD total alkaloids extract solution (0.196 mg·mL-1) were administered to the corresponding treatment group by gavage once a day for 4 weeks, respectively. Rats of the normal group and the model group were given equivalent amount of normal saline by gavage once a day for 4 weeks. The treatment course was 4 weeks. The expression of TGF-β1 mRNA of the liver tissues was detected by FQ-PCR. And the protein ex-pressions of Smad3 and Smad7 were detected by western blotting analysis. The results showed that compared with the model group, there was no significant difference in the expression of Smad7 protein between the total glyco-sides group and the model group, as well as no significant difference between the total alkaloids group and the model group. Expressions of TGF-β1 mRNA and Smad3 protein of other treatment groups were significantly re-duced. And the expressions of their Smad7 protein were significantly increased (P < 0.05 or P < 0.01). It was concluded that crude polysaccharide an d total glycosides fractions were the effective parts of XSD for regulating TGF-β/Smad pathway.