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通过调节LOX-1激素,西斯普拉丁诱导的氧化应激,细胞亡,以及冠状细胞中的促炎反应

Chin-Hsien Wu¹, Wan-Ching Chou^1,2, I-Ming Jou¹

¹Department of Orthopedics, E-Da Hospital, I-Shou University, Kaohsiung City, Taiwan, ROC.

Journal of orthopaedic surgery and research

|February 26, 2025

概括

西斯普拉丁化疗通过增加氧化应激和激活红细胞中的LOX-1/p38/NF-κB通路来降低生长板的高度. 阻断LOX-1或MAPK信号减轻了这种西斯胺诱导的慢性细胞亡.

科学领域:

生物化学生物化学
细胞生物学细胞生物学
在瘤学瘤学.

背景情况:

西斯是一种重要的化疗剂,已知对儿科癌症生长板的影响.
青诱导的生长板功能障碍的确切机制,特别是状细胞损伤,尚未完全理解.
甲状腺素样氧化低密度脂蛋白受体-1 (LOX-1) 涉及骨关节炎和动脉样硬化,调节软骨平衡,但其在思丁作用中的作用尚不清楚.

研究的目的:

阐明西斯丁损害胆红细胞的机制.
调查LOX-1在西斯普拉丁诱导的状细胞损伤和亡中的作用.
为了确定涉及 cisplatin 对生长板状红细胞的影响的特定信号通路.

主要方法:

利用TC28a2细胞来模拟西斯普拉丁诱导的冠状细胞损伤.
施用西斯普拉丁和观察到对活性氧物种 (ROS) 度和MAPK酸化 (p38,ERK) 的影响.
研究了NF-κB信号通路的激活.
采用LOX-1小干扰RNA (siRNA) 和基激活蛋白激酶 (MAPK) 抑制剂,以评估它们对西斯胺诱导的亡的影响.

主要成果:

西斯普拉丁显著增加了ROS水平和p38/ERK酸化,以剂量依赖的方式.
西斯普拉丁治疗导致了体细胞中NF-κB的激活.
用LOX-1 siRNA减弱的传染物引起的西斯普拉丁诱导的亡.
抑制LOX-1或MAPK信号通路减少了西斯胺介导的慢性细胞亡.

结论:

齐斯普拉丁诱导的冠状细胞亡和生长板功能障碍通过LOX-1/p38/NF-κB信号通路进行介导.
洛克斯-1在暴露于西斯普拉丁的软细胞中中介氧化应激和亡方面发挥着至关重要的作用.
准LOX-1/MAPK/NF-κB通路是一个潜在的治疗策略,可以减轻西斯普拉丁对生长板的不良影响.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.西斯普拉丁 (Cisplatin) 是一种洛克斯-1号机场这是一种N-乙囊氨酸.氧化应激是一种氧化应激.

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