针切术激活PI3K/Akt信号通路,通过FGF7,10/KDR轴调节细胞亡
Jia-Ming Qian1, Xiao-Le Wang1, Ting Fang1
1Affiliated Hospital of Jiangxi University of Chinese Medicine, Nanchang, Jiangxi, 330006, People's Republic of China.
Journal of pain research
|January 13, 2026
概括
宫脊椎病 (CS) 的针切术治疗通过FGF7,10/KDR信号轴有效调节细胞亡,激活PI3K/Akt通路. 这种机制阐明了针术是如何修复肌肉和治疗CS骨疾病的.
科学领域:
- 整形外科 整形外科 整形外科
- 分子生物学分子生物学
- 传统中国医药 传统中国医药
背景情况:
- 宫脊椎病 (CS) 是一种常见的疾病,治疗机制尚不清楚.
- 针切除术是一种有效的CS临床治疗方法,通常被描述为"调节肌肉以治疗骨疾病".
- 精确的分子机制背后的针术在CS的疗效仍然在很大程度上是未知的.
研究的目的:
- 阐明针切除术在治疗宫脊椎病 (CS) 的分子机制.
- 调查宫肌细胞亡和PI3K/Akt信号通路的作用.
- 探索FGF7,10/KDR信号轴,调解针术对CS的影响.
主要方法:
- 通过X射线和电子显微镜验证的CS大鼠模型的构建.
- 使用免疫光和COIP进行蛋白质相互作用 (FGF7,FGF10,KDR) 的评估.
- 评估运动和感官功能,病理变化和分子表达 (qPCR,西方斑).
主要成果:
- 针切除术改善了CS大鼠的运动和感觉功能,并减少了宫退行.
- 在CS中,FGF7,10/KDR信号轴和PI3K/Akt路径都涉及到CS.
- 针刺术逆转了改变的蛋白质表达,KDR敲击降低了治疗效果.
结论:
- 针切术通过FGF7,10/KDR信号轴激活PI3K/Akt路径.
- 这种激活调节宫肌细胞亡和肌肉修复.
- 这一途径代表了在治疗CS时针切除术的关键分子机制.
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