| Objective: To investigate the mechanism of STF-083010 in autophagy in TAA-induced oxidative stress,inflammation and liver injury.Methods:The liver injury condition and the expression of IRE1α-s XBP1 signaling pathway was assessedin TAA-induced liver injury.The detection indexes included serum ALT,HE,Ly6 G,CD11b and TUNEL staining.Western Blot was used to detect IRE1α,p-IRE1α,s XBP1,etc.in tissues or cells.The IF1αRNase inhibitor STF-083010 inhibition assay was used to verify its immunoregulatory function.The expression of autophagy-related markers was detected to analyze the role of autophagy in the mechanism of STF-083010 in inhibiting TAA-induced liver injury.Results:Thedegree of liver injury induced by TAA gradually increased with time,serum ALT increased gradually,and HE,Ly6 G and CD11 b positive cells in liver sections also increased with time.TUNEL staining showed that the necrotic area of cells increased gradually.During this process,the IRE1α-s XBP1 signaling pathway is involved in the development of TAA-induced acute liver injury.The use of the IRE1αRNase inhibitor STF-083010 can alleviate TAA-induced oxidative stress and liver inflammation.The mechanism by which STF-083010 inhibits TAA-induced liver injury is mainly through activation of autophagy in the liver.Conclusions:The IRE1α-s XBP1 signaling pathway is involved in the development of acute liver injury induced by thioacetamide(TAA).STF-083010,a specific inhibitor of IRE1αRNase,can inhibit TAA-induced oxidative stress and hepatic inflammation.The mechanism is mainly through activation of autophagy in the liver. |