| Summary: | 碩士 === 國立高雄大學 === 運動健康與休閒學系碩士班 === 99 === In this study, we evaluate the anti-apoptosis pathway of lipoic acid under lipopolysaccha- ride oxidative stress in mouse skeletal cell line (C2C12). The mature myotubes were different- iated from C2C12 cells growth on 10% horse serum differentiation medium 3-5 days. The result of western blotting shows the level of phosphorylate Akt and Bcl-xL protein was incre- ased in the 5μM, 50μM and 0.5mM of lipoic acid treatment and the protein level was decreas- ed especially in 5mM and 10mM lipoic acid treatment. Therefore, the level of phosphorylate Akt and Bcl-xL protein was decreased at the 4, 5 hours treatment. It was shown the high dose and long-term treatment of lipoic acid may induce toxicity in myotubes, but low dose of lipoic acid may protect cells from damage. On the other hand, the phosphorylate Akt and Bcl-xL proteins were decreased by after treatment of lipopolysaccharide, especially in the dosage of 20μg/ml. Moreover, the level of TLR4 protein was expressed after lipopolysaccharide treatm- ent. These results show that oxidative stress of lipopolysaccharide in myotubes were induced by TLR4 protein and may induce oxidative stress by lower the express of phosphorylate Akt and Bcl-xL proteins. Furthermore, the level of Bcl-xL was inhibited after treatment with LY294002. It shows the express of Bcl-xL was regulated by p-Akt. Our results also show after treatment of lipopolysaccharide, lipoic acid can not affect the express of p-Akt and Bcl-xL in myotubes containing LY294002. According to our results, it shows that lipoic acid could against myotubes from oxidative stress by enhancing the express of p-Akt and Bcl-xL protein. It is indicated the lipoic acid against myotubes from lipopolysaccharide stress by PI3K/Akt pathway.
|
|---|
