Effect Of HNF4α Expression In Hepatocytes From Human Hepatitis B Cirrhosis On Hepatocellular Regeneration

Objective:Hepatocyte nuclear factor(HNF4α)is a transcription factor that regulates liver development and the expression of specific genes and is highly expressed in liver cells.However,as a transcription factor enriched in hepatocytes,the relationship between the level of HNF4αin hepatitis B cirrhosis and hepatocyte proliferation remains unclear.In this study,we studied the expression of HNF4αin normal liver tissues and liver cirrhosis with different degree of sclerosis,and analyzed the correlation between the expression of HNF4αand the proliferation activity of liver cells,the degree of cirrhosis and the cell cycle of liver cells,to explore the effect of HNF4αexpression level on hepatocellular regeneration in liver cirrhosis.Methods:This study between January 2018 and December 2020 in Inner Mongolia medical university affiliated hospital Gan Dan Yi spleen surgery in hospital liver resection and liver specimens of 50 cases as the research object,on the basis of Laennec cirrhosis group classification system,detection of liver cells in the liver tissue HNF4 alpha,ki67,c-myc and cyclin D1 expression level,compare different degree of hardening of the liver tissue of the above factor expression in liver cells,differences and correlation analysis of HNF4 alpha expression and the degree of liver cirrhosis,liver cell proliferation activity and the relationship between the cell cycle related factors.Results:1.HNF4α was expressed in all hepatocytes and was localized to the nucleus and was brown in color.The level of HNF4αin mild sclerosis was lower than that in moderate sclerosis,while the level of HNF4αin moderate sclerosis was lower than that in normal liver,and the difference was statistically significant(X~2=11.750,P=0.003).2.Ki67 is expressed in some hepatocytes and is confined to the nucleus and is brown in color.The level of ki67 in mild sclerosis was higher than that in moderate sclerosis,and the level of ki67 in moderate sclerosis was higher than that in normal liver,with statistically significant differences among all groups(X~2=29.184,P<0.001).3.C-myc is expressed in some hepatocytes and is confined to the nucleus and is brown in color.The level of c-myc in mild sclerosis was higher than that in moderate sclerosis,and the level of c-myc in moderate sclerosis was higher than that in normal liver,with statistically significant differences among all groups(X~2=16.067,P=0.001).4.Cyclin D1 is expressed in some hepatocytes and is located in the nucleus and is brown in color.The levels of CYCLIND1 in normal liver tissues,mild and moderate sclerosis of hepatitis B were similar,and there was no statistically significant difference(X~2=3.607,P=0.165).5.Spearman correlation test showed that HNF4αwas negatively correlated with Ki67 and c-Myc in normal liver tissues(r=-0.763,P=0.010;R=0.903,P<0.001),and there was no correlation between HNF4αand Cyclin D1(P=0.584);There was a negative correlation between HNF4αand Ki67 and c-Myc in mild hepatitis B cirrhosis(r=-0.571,P=0.005;R=-0.435,P=0.043),and there was no correlation between HNF4αand Cyclin D1(P=0.165).There was a negative correlation between HNF4αand Ki67 and c-Myc in the liver tissue of moderate hepatitis B sclerosis(r=-0.496,P=0.036;R=-0.591,P=0.010).There was no correlation between HNF4αand Cyclin D1(P=0.760).Conclusion:1.The proliferation activity of hepatocytes in the liver cirrhosis of hepatitis B is higher than that in the normal liver tissue,and the proliferative activity of hepatocytes in human hepatitis B cirrhosis tissues gradually decreases with the aggravation of the degree of cirrhosis.2.HNF4αis involved in the regulation of hepatocellular regeneration in human hepatitis B cirrhosis by changing its expression level,and acts as an inhibitory factor to regulate hepatocyte proliferation in hepatocellular regeneration.3.The expression level of HNF4αwas negatively correlated with c-myc.HNF4αmay play a role in hepatocellular regeneration in human hepatitis B cirrhosis by regulating the cell cycle progression of hepatocytes and thereby regulating the proliferation of hepatocytes by affecting c-myc.