[Oxymatrine alleviates oxidative stress in fat-induced insulin resistance mice by suppressing p38MAPK pathway]

This paper was aimed to investigate the effect of oxymatrine on fat-induced insulin resistance mice（IR）, and to explore the effects of oxymatrine on oxidative stress and on p38 mitogen activated protein kinase (p38MAPK) pathway. ApoE-/- mice with high fat diet for 16 weeks were selected as IR animal model and randomly divided into the model group, oxymatrine 25, 50, 100 mg•kg⁻¹ group. C57BL/6J mice were selected as the normal control group. Mice were gavage for 8 weeks. Fasting blood glucose (FBG), cholesterol (TC), triglyceride (TG), fatty acid (FFA) and serum insulin (FINS) in the plasma were detected. Activity of superoxide dismutase (SOD), glutathione peroxidase, glutathione peroxidase (GSH-Px) and content of malondialdehyde (MDA) in liver were detected. Reactive oxygen species (ROS) content in liver cells were detected by Flow cytometry. The expression of heme oxygenase-1(HO-1), γ-glutamyl cysteine synthetase (γ-GCS) of liver was examined by Real time PCR and Western blot. The protein expression of p38MAPK, p-p38MAPK was examined by Western blot. In the study, the authors found that oxymatrine reduced the levels of FBG, TC, TG and FFA, increased SOD and GSH-Px contents, decreased MDA and ROS content. Compared with model group, HO-1, γ-GCS mRNA and protein expression significantly increased in 50, 100 mg•kg⁻¹ oxymatrine group. The expression of p-p38MAPK decreased in oxymatrine group. The results showed that oxymatrine alleviate oxidative stress in hepatic by inhibiting the phosphorylation of p38MAPK, to ameliorate fat-induced insulin resistance mice.