Influence of hepatic oval cell on the expression of ERK and P38MAPK signaling pathway protein in liver tissue of murine hepatofibrosis

Abstract

Objective To observe the influence of hepatic oval cell （HOC） on the expression ERK and P38MAPK signaling pathway protein in liver tissue of murine experimental hepatofibrosis （HF）.Method SD rats were fed with 10% ethanol and food with high-fat and low-protein, and were injected subcutaneously with carbontetrachloride once every four days for 8 weeks to establish hepatic fibrosis. HOGs were isolated from male HF rats by collagenase porfusion of the liver. HF rats at 8th week were transplanted with 0. 5 ml HOC suspension medium at a density of 1 × 109 cell /ml via portal vein, and the rats were sacrificed at 8th, 15th, 30th day respectively. Histopathologic changes of liver tissues were observed by HE and Masson. The expression of ERK and P38MAPK signaling pathway protein were determined by Western blotting. Result Hepatofibrosis was reversed and the degree of hyperplasia fibrilcollagen in hepatic fibrosis rats decreased significantly by HOC transplantion. HOC down-regulated the protein expression of Ras, ERK,p-ERK, c-fos, c-jun, STAT3, ALB, FGF-3, PCNA （ F = 91.88,36.28,54.66,93.07,64.76,58.49,52.63,20.45 ,27.03, all P 〈 0.05 ）, up-regulated the protein expression level of HNF-α1, PDGF-Rβ significantly in liver tissues（F = 18.63,25.99,P 〈0.05）. Conclusions HOC improves the degree of hepatofibrosis through inhibiting hyperplasia of collagen fibril in liver tissue of hepatofibrosis rats. With the presence of HOC the expression of c-fos,c-jun,STAT3,5 was not activated by p-P38MAPK. The expression of c-kit and HNF-1α increased and that liver tissue injury alleviated, and hepatofibrosis was improved. Key words: Hepatocytes; Liver cirrhosis; Extracellular regulated protein kinases; Mitogenactivated protein kinases