朱道立, 王康乐, 陈佩林, 沈威. ATP对大鼠成肌细胞抗H2O2凋亡模型分析[J]. 北京工业大学学报, 2013, 39(2): 314-320.
    引用本文: 朱道立, 王康乐, 陈佩林, 沈威. ATP对大鼠成肌细胞抗H2O2凋亡模型分析[J]. 北京工业大学学报, 2013, 39(2): 314-320.
    ZHU Dao-li, WANG Kang-le, CHEN Pei-lin, SHEN Wei. Analysis of ATP on H2O2 Apoptosis Model Resistance in Rat Myoblast Cells[J]. Journal of Beijing University of Technology, 2013, 39(2): 314-320.
    Citation: ZHU Dao-li, WANG Kang-le, CHEN Pei-lin, SHEN Wei. Analysis of ATP on H2O2 Apoptosis Model Resistance in Rat Myoblast Cells[J]. Journal of Beijing University of Technology, 2013, 39(2): 314-320.

    ATP对大鼠成肌细胞抗H2O2凋亡模型分析

    Analysis of ATP on H2O2 Apoptosis Model Resistance in Rat Myoblast Cells

    • 摘要: 为了探讨解决L6大鼠成肌细胞被H2O2损伤的问题,分别用1.210 48、2.420 96、4.841 92 g/L ATP溶液对成肌细胞处理后,利用MTT法、流式细胞仪和荧光凋亡抗体检测了细胞损伤程度.结果表明,经H2O2损伤后L6成肌细胞存活率明显降低,凋亡率增加.各种剂量ATP溶液均能提高L6成肌细胞的存活率,促使抗凋亡因子bcl-2表达增加,促凋亡因子bax表达降低,减少凋亡的发生.其保护程度随ATP溶液剂量的减少而增强,在1.210 48 g/L剂量时效果最为显著.ATP溶液对H2O2诱导损伤的L6大鼠成肌细胞具有明显保护作用,其机制是通过mTOR/STAT3信号通路增强凋亡抑制因子bcl-2表达、抑制凋亡促进因子bax表达,从而与抑制细胞凋亡有关.

       

      Abstract: To solve the hydrogen peroxide(H2O2) damage of L6 rat myoblast cells,adenosine triphosphate(ATP) solution of 1.210 48,2.420 96,and 4.841 92 g/L were used to treat myoblast cells,and MTT method,flow cytometry,DAPI fluorescence staining,HE staining and immunocytochemistry fluorescent apoptotic antibody were applied to test the damage.Results show that L6 myoblast cells are damaged by H2O2,the cells survival rate significantly decreases and the apoptosis rate increases.The survival rate of L6 myoblast cells increases with the concentrationes of each ATP solution,the expression of bcl-2 is promoted to increase and the expression of bax decreases to reduce the incidence of apoptosis.The degree of protection increases with decreasing ATP concentration.The effect is the most obvious in the dose of 1.210 48 g/L.The ATP solution has comparable protective effect of myoblast cells on H2O2-induced injury.The main mechanism of ATP solution is related to strengthen the expression of bcl-2 and inhibit that of bax through mTOR/STAT3 signal transduction with inhibiting apoptosis of cells.

       

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