[Animal modeling] The effect of -N-acetylcysteine on liver oxidative stress and FoxO1 activity in type 2 diabetic rats

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

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

  Results: Compared with group C, plasma TG, FFA, AST, ALT, MDA, and liver tissue MDA content, Caspase-3 expression level, and FoxO1 activity level in group D rats increased significantly, while SOD, CAT, and liver tissue levels were significantly increased. Both ATP level and GSH-Px activity were significantly reduced; NAC treatment can inhibit the changes of the above indicators in diabetic rats after 8 weeks, and the difference is statistically significant.

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