The Relationship Between PI3K / AKTPathway and Intestinal Flora Confirmsthe Liver-Gut Axis Theory to Evaluate theMechanism of POP Inhibition Of APAPInduced Acute Liver Injury in Mice

Abstract

Background: The purpose of this study was to investigate the relationship between PI3K / AKT pathway and intestinal flora, and the liver-gut axis theory was confirmed to evaluate the mechanism of POP inhibition of APAP induced acute liver injury in mice.
Methodology: Liver tissue H&E, TUNEL, Hoechst 33,258, immunofluorescence staining, western blot method was used and intestinal flora were tested to comprehensively evaluate the protective mechanism and therapeutic effect of POP on liver injury induced by single injection of APAP (250 mg / kg) in mice.
Results: POP could increase the proportion of Lactobacillus and decrease the abundant of norank_o_Clostridiales and Prevotella compared with APAP induc tion liver injury in the intestine of mice. POP pretreatment could reverse GSH depletion and CYP2E1 overexpression, reduce the expression of MDA and 4-HNE, and decrease the contents of ALT, AST, TNF-α and IL-1β, while the related proteins of PI3K / AKT signaling pathway are also close to the level of normal control group. POP pretreatment was significantly to reduce APAP-induced liver tissue apoptosis, necrosis and inflammatory infiltration.
Conclusion: The PI3K/AKT pathway-mediated Bax/Bcl-2 and NF-κB signal cascade was blocked and interfered by POP, which was shown by protecting the structure of intestinal flora and repairing the mice intestine mucosa to suppress the oxidative stress of liver tissue, improve the inflammatory response and reduce liver cell apoptosis and necrosis.