【Animal modeling】-Effect of N-acetylcysteine on hepatic oxidative stress and FoxO1 activity in type 2 diabetic rats

  Objective: To investigate the effect of antioxidant N-acetylcysteine on hepatic oxidative stress and FoxO1 activity in type 2 diabetic rats.

  Methods: Twenty-four male SD rats were randomly divided into normal control group (C), non-diabetic diabetes treatment group (D) and NAC treatment group (D + NAC) (n=8). STZ) and high-fat diet to establish a rat model of type 2 diabetes. The D+NAC group was given NAC 1.5 g/kg by gavage every day, and the C and D groups were given the same volume of normal saline. After 8 weeks, the automatic biochemical analyzer Plasma triacylglycerol (TG), free fatty acid (FFA), aspartate aminotransferase (AST), alanine aminotransferase (ALT) levels were detected, and kits were used to detect liver tissue superoxide dismutase (SOD), catalase (CAT) The levels of glutathione peroxidase (GSH-Px), adenosine triphosphate (ATP) and the content of lipid peroxide malondialdehyde (MDA) in plasma and liver tissue; Western blot analysis of the expression level of Caspase-3 in liver tissue, and The expression levels of FoxO1 protein in the cytoplasm and nucleus were analyzed to indirectly reflect the activity level of FoxO1.

  RESULTS: Compared with group C, the levels of TG, FFA, AST, ALT, MDA and MDA in liver tissue, expression level of Caspase-3, and activity of FoxO1 in group D were significantly increased, while SOD, CAT, and SOD in liver tissue were significantly increased. ATP level and GSH-Px activity were significantly decreased; NAC treatment for 8 weeks could inhibit the changes of the above indexes in diabetic rats, and the difference was statistically significant.

  Conclusion: Antioxidant NAC can alleviate diabetes-related liver function damage, and its mechanism may be related to its inhibition of diabetic oxidative stress level, mitochondrial dysfunction and FoxO1 overactivation.