登德罗氧化物通过AKT/mTOR信号通路减轻NRK-52E细胞中高葡萄糖诱导的氧化损伤
Song Hee Lee1, Ju Ri Kim1, Joo Kyung Shin1
1School of Pharmacy, Sungkyunkwan University, Seobu-ro 2066, Kyunggi-Do, Suwon, Republic of Korea.
Planta medica
|December 1, 2023
概括
氧化物 (DPx) 通过减少氧化应激,保护细胞免受高葡萄糖损伤. 这种天然化合物显示出治疗糖尿病病的前景.
科学领域:
- 腎臟病學 (nephrology) 是一種醫學專業.
- 药理学 药理学是指药理学的学科.
- 生物化学 生化学
背景情况:
- 糖尿病病是一种主要的糖尿病并发症,由高血糖驱动.
- 氧化 (DPx) 是一种天然化合物,已显示出各种生物效应,但其在损伤中的作用尚不清楚.
研究的目的:
- 研究DPx在脏管状上皮细胞中对高葡萄糖诱导的细胞毒性的保护机制.
- 探索DPx作为糖尿病病治疗剂的潜力.
主要方法:
- 管状上皮细胞NRK-52E细胞被用正常葡萄糖,高葡萄糖 (HG),HG + 甲福林或HG + DPx治疗.
- 分析了细胞循环,细胞亡,甲基 (MDA),高级糖化终产物 (AGEs),活性氧物种 (ROS) 和毒性生物标志物 (KIM-1, PKM2, SBP1, NGAL).
主要成果:
- 高葡萄糖显著增加了MDA,AGE和ROS水平,这些水平被DPx和甲胺降低.
- DPx治疗降低了HG治疗细胞中的KIM-1,PKM2,SBP1和NGAL水平.
- DPx增强了抗氧化酶活性,并可能通过AKT/mTOR信号通路起作用.
结论:
- 登德罗氧化物 (DPx) 对高葡萄糖诱导的管细胞损伤具有保护作用.
- DPx的机制涉及抑制氧化应激,可能通过AKT/mTOR途径.
- DPx是管理高葡萄糖诱导的糖尿病病的潜在治疗候选者.
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