Expression changes of Akt and GSK-3β during vascular inflammatory response and oxidative stress induced by high-fat diet in rats

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DOI: 10.4236/jbise.2013.65A001    2,577 Downloads   4,510 Views  Citations

ABSTRACT

Aim: To observe the expression changes of Akt and GSK-3β during vascular inflammatory response and oxidative stress induced by high-fat diet in rats. Methods: 20 male Sprague-Dawley rats were separately fed for 18 weeks with two types of diets; a normal diet (control group, CON) or high-fat diet hyperlipidmia group, HLP). Then the body weight, lipid parameter, plasma hepatocyte growth factor (HGF), serum superoxide dismutase (SOD) , malondialdehyde (MDA), Tumor necrosis factor-α (TNF-α), a Soluble intercellular adhesion molecule-1 (sICAM-1), Lectin-like oxidized cellulose low density lipoprotein receptor-1 (LOX-1), as well as aortic endothelial p-GSK-3β, GSK-3β, p-Akt, Akt expressions were determined. Results: In comparison with the control group, the model group showed a significant increase in the levels of serum total cholesterol (TC), triglyceride (TG), low density lipoprotein cholesterol ( LDL-C) and significant decrease in the level of serum high density lipoprotein cholesterol (HDL-C) after high-fat diet for 18 weeks (p < 0.05 or p < 0.01). Meanwhile, a more obvious increase of plasma HGF, LOX-1 and serum MDA, TNF-α, and sICAM-1 levels were observed relative to the control group (p < 0.05 or p < 0.01). Moreover, high-fat diet significantly increased the phosphorylation of Akt and GSK-3β in rat aorta. Conclusion: Short-term high-fat diet could induce vascular endothelium injury by increasing inflammation and oxidative stress. And PI3K/Akt pathway could play an important role in hyperlipidemia-induced vascular endothelium injury.

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Wang, J. , Yin, H. , Huang, Y. , Guo, C. , Xia, C. and Zhang, L. (2013) Expression changes of Akt and GSK-3β during vascular inflammatory response and oxidative stress induced by high-fat diet in rats. Journal of Biomedical Science and Engineering, 6, 1-5. doi: 10.4236/jbise.2013.65A001.

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