[Cordyceps mycelia extract decreases portal hypertension in rats with dimethylnitrosamine-induced liver cirrhosis: a study on its histological basis].

Objective: To study the effects of Cordyceps mycelia extract (CME) on portal hypertension in rats with dimethylnitrosamine (DMN) induced liver cirrhosis and probe into the mechanism of the action.
Methods: A rat model of liver cirrhosis was induced by peritoneal injection of DMN (at a dose of 10 microg/kg, once a day, 3 consecutive days per week) for 4 weeks. Other 15 rats were assigned into normal control group. The rats in CME-prevented group were administrated CME 0.74 g/(kg.d), once a day, simultaneously with DMN treatment and kept on 4-week administrating, and the rats in CME-treated group were administrated after the model was established. After 3-day, 2- and 4-week DMN injection and 2-, 4-week after the rat liver got cirrhosis, the pressure of portal vein (Ppv) was directly measured by intubation via tributary of vena mesenteric anterior. The serum hyaluronic acid (HA) content was measured by radioimmunoassay. The expressions of CD44, von Willebrand factor (vWF), laminin (LM), alpha-smooth muscle actin (alpha-SMA), type I collagen (Col I) and type IV collagen (Col IV) proteins in the hepatic sinusoida l walls were examined by immunohistochemistry.
Results: The caliber of portal vein (Cpv) and Ppv in the CEM group (after 4-week prevention) were significantly decreased as compared with those in the untreated group at the same point of time (P<0.05), also including serum HA content (P<0.05), and vWF, Col I, Col IV, LM, alpha-SMA positive staining (P<0.05); however, CD44 positive staining were increased in the CEM group (P<0.05). The Cpv, Ppv and serum HA content were significantly decreased after 2-week CME treatment as compared with those in the untreated group (P<0.05). After 4-week CME treatment, the Cpv and Ppv in the CEM group were recovered to the normal level. After 2- and 4-week CME treatment, vWF, Col I, LM and alpha-SMA positive stainings were decreased (P<0.05), and CD44 positive staining was increased (P<0.05) in the CME group as compared with those in the untreated group at the same point of time, but there were no marked changes found in Col IV staining.
Conclusion: CME plays a good role in preventing and treating the portal hypertension in rats with DMN-induced liver cirrhosis. The histological bases of the effects are to treat liver sinusoida l endothelial cell injury, inhibit hepatic stellate cell activation, inhibit and reverse hepatic sinusoida 1 capillarization.