摘要
目的:验证骨骼肌白细胞介素6(interleukin6,IL-6)基因转录的增加可能与c-Jun氨基末端激酶(c-Jun NH2-terminal kinases,JNK)信号通道的激活有关,并且探讨运动前肌糖原含量是否影响收缩骨骼肌JNK信号通道的激活。方法:大鼠先进行糖原消耗运动,在恢复期24h内采取不同的膳食干预手段,使大鼠在下一次定量运动前骨骼肌肌糖原含量不同。结果:运动时,血浆IL-6浓度、骨骼肌IL-6mRNA及核磷酸化JNK含量均显著上升,运动后恢复期降低;在相同时间点,低糖原组血浆IL-6浓度及骨骼肌IL-6 mRNA均显著高于正常糖原组;在相同时间点,核磷酸化JNK含量在低糖原组与高糖原组之间没有显著性差异。结论:收缩骨骼肌中,IL-6基因转录可能与低糖原含量及JNK信号通道的激活有关,然而,低糖原促进的IL-6基因转录可能不是通过激活JNK信号通道。
Object.. To test the hypothesis that the increase of IL-6 gene transcription was possi- bly related to the activation of JNK kinase signaling pathway during contraction in skeletal muscle and determine whether glycogen availability influences the activation JNK signaling in contracting skeletal muscle. Methods~ rats were firstly exercised to deplete glycogen of skeletal muscle, then meal interference were adopted in the 24h recovery after exercise to obtain different glycogen content before the next fix quantity exercise. Results： the level of plasma IL-6, the IL-6 mRNA and nuclear phospho-JNK content in rats markedly elevated （P〈 0：05）, and then decrease in the recovery of post-exercise; the level of plasma IL-6 and IL-6 mRNA in rats of low glycogen group were significant higher than that of rats in normal glycogen group （P〈 0. 05） in certain time point; the phospho-JNK content in rats had not difference with low Glycogen group and normal glycogen group in same time point. Conclusion.. IL-6 gene transcription was possibly related to the activation of JNK kinase signaling pathway during contraction in skeletal muscle, and the increase in phosphorylation of JNK in the nucleus was not through activation of JNK signaling pathway.
出处
《体育科学》
CSSCI
北大核心
2007年第10期69-74,共6页
China Sport Science
基金
国家科技攻关计划项目(2002BA904B04)
国家自然科学基金项目(30570897)
关键词
低肌糖原
IL-6
JNK信号通道
骨骼肌
鼠
动物实验
low muscle glycogen content
IL- 6
J NK signaling pathway
skeletal muscle
rats animal experiment
