ABSTRACT
<p><b>OBJECTIVE</b>To study the mechanism of Corydyceps polysaccharide (CP) actions against liver fibrosis.</p><p><b>METHOD</b>SD rats were randomly divided into normal control group, DMN-induced liver fibrosis model group and CP treated group. Model group and CP group were injected intraperitonealy with 0. 5% dimethylnitrosamine (DMN) at dose of 2 mL x kg(-1) for 4 weeks to induce liver fibrosis. Then the later group was orally taken CP for 4 weeks. Liver tissue hydroxyproline (Hyp) content was determined by Jamall's method. The liver serum of ALT and AST activities, level of albumin and total bilirubin were analyzed The liver collagen deposition and were observed with Masson' collagen stains. In addition,the tissue inhibitor of metallprteinase-2 (TIMMP-2) level, metalloproteinade-2 (MMP-2) activity, type IV collagen content were observed. Liver samples were also analyzed malondiadehyde (MDA)level and superoxide dismutase (SOD) activity.</p><p><b>RESULT</b>Compare with model group, CP improved the hepatic function (ALT, AST, Alb and Tbil). There were significant decreased of MDA content in CP group, SOD of CP group were markedly increased. Compared to those of normal control group, Hyp content, IV collagen content, TIMMP-2 level in liver tissue of model group increase significantly, and MMP-2 activity decreased, while CP decrees these pathological increase at different degrees.</p><p><b>CONCLUSION</b>CP exerts rather good action against liver fibrosis, and with the mechanism relating to improve degradation of the deposited collagens and anti-lipid peroxiation.</p>
Subject(s)
Animals , Male , Rats , Collagen Type IV , Metabolism , Cordyceps , Chemistry , Dimethylnitrosamine , Hydroxyproline , Metabolism , Liver , Metabolism , Pathology , Liver Cirrhosis , Metabolism , Malondialdehyde , Metabolism , Matrix Metalloproteinase 2 , Metabolism , Polysaccharides , Pharmacology , Random Allocation , Rats, Sprague-Dawley , Superoxide Dismutase , Metabolism , Tissue Inhibitor of Metalloproteinase-2 , MetabolismABSTRACT
<p><b>OBJECTIVES</b>To study the role of hepatic sinusoid capillarization during the formation of portal hypertension in fibrotic rats induced by dimethylnitrosamine (DMN).</p><p><b>METHODS</b>Hepatic fibrotic rats were induced by administration of DMN intraperitoneally three times a week for 4 weeks. The rats were harvested on day 2 and weeks 1, 2, 3, 4, 5, 6, 8, 12 and 24. The formation of liver fibrosis and hepatic sinusoid capillarization were observed by morphologic methods. Pressure of portal vein (Ppv) was directed measured with intubation tube method by mesentry anterior vein.</p><p><b>RESULTS</b>The Ppv was getting higher and higher with the administration of DMN. After four weeks, the Ppv was higher than that of control [(1.10+/-0.18)kPa vs (0.52+/-0.04)kPa, t=6.41, P<0.01]. The dynamic change of hepatic sinusoid capillarization was in accordance with that of Ppv, which normalized gradually after the DMN was stopped. Significant positive correlation existed between the dynamic change of Ppv and the expression of vWF, laminin and alpha-SMA in sinus (r=0.833, P<0.01; r=0.953, P<0.01; r=0.919, P<0.01).</p><p><b>CONCLUSION</b>Hepatic sinusoid capillarization is the vital cause for portal hypertension in fibrotic rats induced by DMN.</p>