Effects of truncation and inversion prescription on content of TNF-α in serum and hepatic tissue and expression of TNFR1 in hepatic tissue for rats with acute-on-chronic liver failure

Objective To observetheeffectsoftruncationandinversionprescriptiononcontentoftumornecrosisfactor-α(TNF-α)inserum andhepatictissueandexpressionoftumornecrosis factor receptor 1(TNFR1) in hepatic tissue for acute-on-chronic liver failure(ALCF) model rats and then analyze its part of action mechanisms on intervention for ACLF.Methods One hundred and fifty Wistar rats were divided into a normal group,a model group and a Chinese medicine group.The rat model of liver cirrhosis or fibrosis was immunologically induced by human serum albumin and then D-galactosamine(D-GaLN) combined with lipopolysaccharide(LPS) were one-off intraperitoneal injected to make an acute attack and establish the rat model of ACLF.The Chinese medicine group was treated by intragastric administration with prescription of truncation and inversion for 3 consecutive days before the acute attack.The rats were sacrificed by anesthesia at the 4th,8th and 12th hour after the acute attack,respectively.The content of TNF-α in serum and hepatic tissue of rats in each group was detected by ELISA method,while the expression intensity of TNFR1 in hepatic tissue was examined by immunohistochemistry.Results Compared with the normal group,the content of TNF-α in serum and hepatic tissue and integrated optical density(IOD) of TNFR1 in hepatic tissue were increased in the model group at every time point,which had a significant difference(P0.05);Compared with the model group at corresponding time point,the content of TNF-α in serum and hepatic tissue and expression of TNFR1 in hepatic tissue were lowered in the Chinese medicine group,which was especially obvious at 4th and 8th hour under comprehensive comparison(P 0.05).Conclusion The reduction of TNF-α content in serum and hepatic tissue,suppression of TNFR1 expression in hepatic tissue,prevention of the dead signal transduction,and inhibition of hepatocyte apoptosis might be one of action mechanisms for truncation and inversion prescription to intervene in ACLF.