Study on the Mechanism of LPS/LBP-TNF-α Signal Pathway Induced by G-SH on Acute Alcoholic Liver Injury

Abstract

Oxidative stress plays an important role on the occurrence and development of acute alcoholic liver injury. Therefore, it is necessary to explore the role and related mechanism of antioxidant Glutathione (GSH) in acute alcoholic liver injury. The animal model of acute alcoholic liver injury in mice was established and divided into different groups, i.e., drug treatment and observation. The body weight and liver weight of mice in each group were recorded, the liver index was calculated, and the pathological changes of liver tissue were observed. The contents of AST, ALT and ALP in serum of mice were detected by automatic analyzer. Liver tissues were extracted to detect oxidative stress indexes such as Superoxide Dismutase (SOD), Glutathione peroxidase (GSH-Px), Catalase (CAT), Malondialdehyde (MDA) and liver function indexes such as TC, TG. TdT-mediated dUTP Nick-End Labeling (TUNEL) was used to detect hepatocyte apoptosis in each group, and Western blot (WB) and Real time quantitative PCR (qPCR) were used to detect the expression of related pathway proteins and apoptotic proteins. Serum Tumor necrosis factor-α (TNF-α), Interleukin-6 (IL-6) and Interleukin-1β (IL-1β) were detected by Enzyme linked immunosorbent assay (ELISA) kit. In addition, we also applied Lipopolysaccharide (LPS) to establish the model of liver injury, and detected that the liver function indexes related to liver injury, apoptosis. The level of oxidative stress and the level of inflammatory factors were used to explore the relationship between GSH and Lipopolysaccharide binding protein (LBP) signal pathway. Results showed that GSH could reduce the indexes of liver function, oxidative stress and the level of inflammatory factors, and also reduce the LPS-induced liver injury in mice. GSH may alleviate alcohol-induced liver injury by inhibiting LPS/LBP-TNF-α signal pathway.