ABSTRACT
Aim To investigate the effects of anisodamine on the pressure of portal vein of experimental liver fibrosis and its mechanisms of action. Methods The experimental liver fibrosis model was produced by CCl_4. The preventive group was treated ten weeks with anisodamine 7.0 mg?kg~(-1) ip once everyday. All therapeutic groups were treated six weeks with anisodamine 7.0 mg?kg~(-1) or 14.0mg?kg~(-1) ip once everyday. After CCl_4 injection for ten weeks, the pressure of portal vein,the content of NO in livers, and liver iNOS and eNOS mRNA expressions were detected with different methods.Results The pressure of portal vein was significantly reduced in anisodamine preventive group and anisodamine therapeutic groups. The liver content of NO and the expression of iNOS and eNOS were all inhibited by the treatment of anisodamine.Conclusion Anisodamine reduced the expressions of iNOS and eNOS to synthesis of NO in liver. As a result, the pressure of portal vein of fibrosis rats decreased. So Portal hypertension of liver fibrosis may be improved by anisodamine in patients.
ABSTRACT
Objective To explore the clinical significances of total antioxidation (TAO) and nitric oxide synthase (NOS) expression in patients with liver diseases.Methods The concentrations of TAO,NOS and nitric oxide(NO) were determined and the mechanism of their changes were analyzed in sera of patients with acute hepatitis(AH),chronic hepatitis(CH),liver cirrhosis(LC) and hepatocellular carcinoma(HCC).Results The abnormal rate of TAO was 80% in AH or in CH,and 50% in LC or in HCC,respectively.The sera NOS activity over normal reference value was 70% in patients with liver diseases.The abnormal rate of NO level was 70% in AH,CH and LC groups,and 48% in HCC,respectively.The average level of serum TAO was significantly higher in AH group or in CH group,but not in both HCC and LC groups than that in normal subjects.The average levels of NO and NOS were significantly higher in patients with liver diseases than those in normal subjects.However,the two markers were lower in HCC patients than those in AH,CH and LC groups,respectively.Conclusions The data suggest that the activity of NOS is close relation to serum NO level in patients with liver diseases,the increase of NO concentration may play a role in protection of hepatocytes.
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Objective To explore the roles of vascular endothelial growth factor (VEGF) in microvessel angiogennesis, development and metastasis of hepatocellular carcinoma (HCC). Methods The expression and cellular distributions of VEGF in HCCs were investigated by immunohistochemical method, and the levels of total RNA and VEGF also were quantitatively analysed in HCCs and paracancerous tissues. Results The positive rates of VEGF were 63 9% in all HCCs, 78 3% in non-encapsuled HCCs, and 90 9% in HCCs with extra-hepatic metastasis, respectively. VEGF expression was not associated with tumor size and differentiation degree. The total RNA level in HCCs was significantly lower than that in paracancerous and distal paracancerous tissues (P
ABSTRACT
Objective To investigate the protective effects and the mechanisms of anisodamine on experimental liver damage. Methods The experimental liver injury model was established by ANIT and CCl 4.Studies were made after ANIT or CCl 4 administration,and the control group compared with the experimental groups which were treated by anisodamine on the pathologic morphology, biochemical indices and the contents of Ca 2+ ,MDA and the ability of total antioxidation in the liver.Effects of anisodamine on sleeping time of the mice toxicated by given sodium phenobarbital were also determined.Results The elevation of ALT, ALP, BiL, CHE and the decrease of serum protein in ANIT or CCl 4 liver damage were significantly improved by treatment with anisodamine .It also remarkably diminished the hepato-cellular and chole-epthelial-cellular degeneration and necrosis induced by ANIT or CCl 4.The contents of Ca 2+ ,MDA and the ability of total antioxidation in the liver were all decreased by treatment with anisodamine. The sleeping time induced by sodium phenobarbital in the toxicated mice was reduced by anisodamine. Conclusion Anisodamine have significant protective effects on liver injury of intrahepatic cholestasis and chemical hepatitis and the mechanism may be associated with blocking M-receptor and enhancing antioxidation and antitoxic activity in liver.
