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探討硫辛酸在骨骼肌細胞對於脂多醣體氧化壓力之保護作用 = Study o...

國立高雄大學運動健康與休閒學系碩士班

探討硫辛酸在骨骼肌細胞對於脂多醣體氧化壓力之保護作用 = Study on the Protective Effects of Lipoic Acid in Skeletal Muscle under Lipopolysaccharide Oxidative Stress

紀錄類型:	書目-語言資料,印刷品 : 單行本
並列題名:	Study on the Protective Effects of Lipoic Acid in Skeletal Muscle under Lipopolysaccharide Oxidative Stress
作者:	陳冠霖,
其他團體作者:	國立高雄大學
出版地:	[高雄市]
出版者:	撰者;
出版年:	民100
面頁冊數:	51葉圖，表格 : 30公分;
標題:	脂多醣體
標題:	Lipopolysaccharide
電子資源:	http://handle.ncl.edu.tw/11296/ndltd/46760388938871731655
附註:	參考書目：葉44-47
摘要註:	本研究將小鼠肌纖維母細胞 C2C12細胞株以含10%馬血清的分化培養液培養3至5天分化為myotube，探討硫辛酸對骨骼肌細胞接受脂多醣體氧化傷害後的抗凋亡路徑。我們藉由西方墨點法分析蛋白質，結果發現，硫辛酸在5 μM、50 μM及0.5 mM作用濃度會增加磷酸化 Akt (p-Akt)與 Bcl-xL蛋白質表現量，但投予5 mM及10 mM硫辛酸會減少 p-Akt與 Bcl-xL蛋白質表現量。此外，硫辛酸在第4、5小時作用時間會減少 p-Akt與 Bcl-xL蛋白質表現量。以上結果顯示，硫辛酸在高劑量與長時間作用下對 myotube可能具有毒性；但低劑量硫辛酸對細胞可能具有保護作用。另一方面，細胞投予脂多醣體則會降低 p-Akt與 Bcl-xL蛋白質表現量，並且在20 μg/mL脂多醣體作用下蛋白質表現量達到最低。此外，Toll-like receptor-4 (TLR4)蛋白質則隨細胞投予脂多醣體而增加。以上結果顯示，脂多醣體透過 TLR4的活化誘發氧化傷害並且會降低 p-Akt與 Bcl-xL蛋白質表現而對 myotube造成傷害。接著將 p-Akt抑制劑 LY294002加入 myotube中抑制 p-Akt後發現 Bcl-xL蛋白質也隨之被抑制，顯示硫辛酸可能經由活化 p-Akt影響 Bcl-xL的表現。另一方面，實驗結果顯示將脂多醣體投予含抑制劑 LY294002的 myotube之後，硫辛酸並無法影響 p-Akt與 Bcl-xL的表現量。而根據實驗結果顯示硫辛酸可藉由提升 p-Akt與 Bcl-xL蛋白質表現量保護 myotube免於氧化傷害。綜合本實驗發現，在 myotube中硫辛酸對脂多醣體引發的傷害可能經由 PI3K/Akt pathway達到保護的效果。 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.

探討硫辛酸在骨骼肌細胞對於脂多醣體氧化壓力之保護作用 = Study on the Protective Effects of Lipoic Acid in Skeletal Muscle under Lipopolysaccharide Oxidative Stress
陳, 冠霖

探討硫辛酸在骨骼肌細胞對於脂多醣體氧化壓力之保護作用 = Study on the Protective Effects of Lipoic Acid in Skeletal Muscle under Lipopolysaccharide Oxidative Stress / 陳冠霖撰 - [高雄市] : 撰者, 民100. - 51葉 ; 圖，表格 ; 30公分.
參考書目：葉44-47.
脂多醣體Lipopolysaccharide

探討硫辛酸在骨骼肌細胞對於脂多醣體氧化壓力之保護作用 = Study on the Protective Effects of Lipoic Acid in Skeletal Muscle under Lipopolysaccharide Oxidative Stress
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