Protective Mechanism Of Endogenous Platelets On D-GalN-induced Acute Liver Injury

Objective To evaluate the protective effect of endogenous platelets on acute liver injury by establishing a model of acute liver injury induced by D-Galactosamine in mice.Methods A mouse model of acute liver injury was induced by intraperitoneal injection of D-Galactosamine.A thrombocytopenic mouse model was induced by intraperitoneal injection of Anti-platelet surface molecule CD41 antibody.A mouse model of thrombocytosis was induced by intraperitoneal injection of recombinant thrombopoietin.The number of platelets and the levels of alanine aminotransferase and aspartate aminotransferase were detected.The pathological changes of liver tissue sections were observed,and the expression of related proteins in liver tissues was detected by Western blot.Results The model of acute liver injury,thrombocytopenia and thrombocytosis were successfully established.Compared with the blank group,the platelet count of the acute liver injury model group was decreased(P<0.01),serum alanine aminotransferase and aspartate aminotransferase were significantly increased(P<0.001).Compared with the liver injury model group,the serum alanine aminotransferase in the thrombocytopenia group,there was no significant difference in aspartate aminotransferase(P>0.05),and serum alanine aminotransferase and aspartate aminotransferase levels were lower in the thrombocytopenia group(P<0.05).Liver pathological biopsy results suggest that liver cells in acute liver injury model group and thrombocytopenia group have different degrees of hepatocyte necrosis,deep nuclear staining,blurred cell boundaries,hepatocyte edema,blurred hepatic lobule structure.The liver pathological changes in the mice with elevated platelets were mild.Western blot showed that the expression of hepatocyte growth factor in the thrombocytosis group was higher than that in the acute liver injury group,and the difference was statistically significant.Conclusion TPO-induced endogenous thrombocytosis has protective effects on acute liver injury induced by D-Galactosamine in mice.Increased expression of HGF by platelets is one of the mechanisms that protect liver cells.