可以防止葡萄糖皮质醇诱导的慢性细胞自:一项体外研究
Qiuru Wang1, Wanli Zhang2, Jian Hu3
1Department of Orthopaedic Surgery, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, P.R. China.
Molecular medicine reports
|August 18, 2023
概括
通过激活PI3K/AKT/mTOR通路来防止葡萄糖皮质类药物诱导的慢性细胞自. 这种干预保护了状细胞的活力,为管理葡萄糖皮质体副作用提供了潜在的治疗策略.
科学领域:
- 细胞生物学 细胞生物学
- 药理学 药理学是指药理学的学科.
- 生物化学 生物化学
背景情况:
- 已知葡萄糖皮质类药物可诱导慢性细胞自,这是一个细胞过程.
- 被认为是自的关键调节剂.
- PI3K/AKT/mTOR信号通路在细胞调节中起着至关重要的作用.
研究的目的:
- 为了研究是否可以预防葡萄糖皮质激素诱导的慢性细胞自.
- 在这种情况下,要确定是否调节PI3K/AKT/mTOR信号通路.
主要方法:
- 鼠类和人类的红细胞被用德甲和不同度的化治疗.
- 使用CYTO-ID®染色和传输电子显微镜评估了自水平.
- 自标记物 (LC3B) 的基因和蛋白质表达和信号通路组件 (AKT,mTOR) 通过RT-qPCR和西红斑分析.
- 细胞活力测量使用细胞计数工具-8测定.
主要成果:
- 德克萨米他诱导了状细胞自,降低了AKT和mTOR表达,并降低了细胞活力.
- 化 (10毫米) 与德克萨米他相结合显著降低了自水平.
- 与单独使用德甲相比,治疗增加了AKT和mTOR的表达,并改善了冠状细胞的活力.
结论:
- 有效地防止葡萄糖皮质类药物诱导的慢性细胞自.
- 这种保护作用是由PI3K/AKT/mTOR信号通路的激活介导的.
- 的使用可以减轻葡萄糖皮质类药物对状细胞活力的负面影响.
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