ABSTRACT
OBJECTIVE: To study the effects of Cordyceps sinensis on dimethylnitrosamine-induced liver fibrosis in rats. METHODS: SD rats were divided into normal control group, untreated group and Cordyceps sinensis-treated group. The rats in each group were fed with corresponding drug for 4 weeks. The rat's liver collagen deposition was observed with collagen staining. Hydroxyproline (Hyp) contents in liver tissue of the rats in 3 groups were determined with HCl hydrolysis. The tissue inhibitor of metalloproteinase-2 (TIMP-2) and type IV collagen contents were observed by Envision, and matrix metalloproteinases-2 (MMP-2) activity was detected by the method of enzyme-picture. Type I collagen was detected by Western blotting. RESULTS: The contents of Hyp, TIMP-2, type IV collagen, and the expression of type I collagen in untreated group were significantly higher than those in the normal control group, while those in Cordyceps sinensis-treated group were significantly lower than those in the untreated group. The content of MMP-2 in untreated group was significantly lower than that in the normal control group, while that in Cordyceps sinensis-treated group was significantly higher than that in the untreated group. CONCLUSION: Cordyceps sinensis can considerably relieve the liver fibrosis, and the mechanism may be related to promoting the degradation of the collagens.
ABSTRACT
<p><b>OBJECTIVE</b>To study the role of hepatic sinusoidal endothelium injury during hepatic fibrogenesis induced by dimethylnitrosamine (DMN) in rats.</p><p><b>METHODS</b>Hepatic fibrosis of rats was induced by administration of DMN intraperitoneally three times a week for 4 weeks. The animals were harvested on day 2 and week 1, 2, 3, 4, 5, 6, 8, 12, and 24. The formation of liver fibrosis and hepatic sinusoid capillarization were successively observed by morphological observation and other methods.</p><p><b>RESULTS</b>Two days after treated with DMN, there was no obvious changes in the liver, but the fenestration of the sinusoidal endothelial cells decreased, and it became more obvious after one week. After four weeks, there was a large necrotic area and a number of pseudolobes appeared. The HA in the serum was lower than that of control (231.30 ng/ml +/- 143.80 ng/ml vs 56.50 ng/ml +/- 18.10 ng/ml; t=3.14, P<0.05), but the hydroxyproline content was obviously higher than that of control (223.04 microg/g +/- 37.09 microg/g vs 61.55 microg/g +/- 20.85 microg/g; t=8.28, P<0.05). Hepatic sinusoid capillarization was gradually formed and defenestration of the hepatic sinusoidal endothelium preceded the appearance of serious hepatocellular damage, hepatic fibrosis and basement membrane.</p><p><b>CONCLUSIONS</b>The damage and phenotypic alteration of the hepatic sinusoidal endothelium may be a vital issue triggering the liver fibrosis induced by DMN.</p>