在西斯普拉丁诱导的HK-2细胞中,CTRP3减弱了炎症,氧化和细胞死亡
Chenglin Zou1,2, Xun Tang1, Tingting Guo1
1Department of Nephrology, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
PeerJ
|August 28, 2023
概括
与C1q/TNF相关的弱交互因子3 (CTRP3) 通过减少氧化应激,炎症和亡,保护免受西斯普拉丁诱导的急性损伤 (AKI). CTRP3可能成为AKI治疗的新疗法标.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 生物化学 生物化学
- 分子生物学分子生物学
背景情况:
- 西斯普拉丁是一种有效的抗瘤药物,但会导致急性损伤 (AKI).
- 氧化应激,炎症和亡是西斯胺诱导的AKI的关键机制.
- 在AKI中,CTRP3的作用仍然不清楚,它是一种具有保护性质的阿迪波金.
研究的目的:
- 调查CTRP3在西斯普拉丁诱导的AKI中的作用.
- 阐明CTRP3保护作用的基础分子机制.
主要方法:
- 在体外实验中使用具有CTRP3过度表达或被淘汰的人类近接管上皮细胞 (HK-2).
- 西斯普拉丁诱导模型AKI.
- 对氧化应激标志物 (MDA,SOD,CAT),炎症性细胞因子 (TNF-α,MCP-1),细胞增殖 (EdU),细胞亡 (Bcl-2,Bax) 和关键信号通路 (Nrf2,MAPK) 的评估.
主要成果:
- 在西斯普拉丁诱导的AKI模型中,CTRP3表达下降.
- 在HK-2细胞中,CTRP3过度表达减弱了西斯普拉丁诱导的氧化应激,炎症和亡.
- CTRP3调节了Nrf2/MAPK信号通路,抑制了MAPK酸化并激活了Nrf2.
- 抑制CTRP3加剧了西斯胺诱导的损伤,而抑制Nrf2或MAPK则逆转了这些影响.
结论:
- CTRP3 具有保护性作用,可以预防西斯普拉丁诱导的 AKI.
- CTRP3通过Nrf2/MAPK通路作用,减轻损伤.
- CTRP3代表了预防或治疗西斯胺诱导的AKI的潜在治疗标.
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