佩林多普里尔阻断Cd诱导的毒性,通过抑制炎症负担,Ang II/Ang 1-7,以及亡信号通路
Zuhair M Mohammedsaleh1, Emad H M Hassanein2, Fares E M Ali3
1Department of Medical Laboratory Technology, Faculty of Applied Medical Sciences, University of Tabuk, Tabuk, 71491, Kingdom of Saudi Arabia.
Biological trace element research
|October 17, 2023
概括
佩林多普利 (PER) 通过减少炎症和亡来保护脏免受 (Cd) 毒性影响. 这项研究表明,PER调节氨酸-血管酶系统 (RAS) 和关键炎症通路,为重金属诱导的损伤提供潜在的治疗益处.
科学领域:
- 毒理学 毒理学 毒理学
- 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.
背景情况:
- (Cd) 暴露会导致严重的损伤,而炎症是其毒性的关键因素.
- 氨酸-动脉素系统 (RAS) 在炎症过程和心血管健康中发挥作用.
- 佩林多普利 (PER) 是一种血管激素转化酶抑制剂,用于高血压和心血管疾病.
研究的目的:
- 调查 (PER) 对 (Cd) 诱导的毒性的保护作用.
- 阐明PER对炎症的影响以及Cd中毒大鼠的潜在分子机制.
- 为了检查PER对 ангиотензин II (Ang II) /Ang-{1-7) 轴和亡途径的调节.
主要方法:
- 鼠被给予1毫克/公斤/天的Perindopril (PER),并暴露于1.2毫克/公斤的单剂量 (Cd).
- 评估了功能 (尿素,肌素,尿酸) 和白尿的血清标志物.
- 评估了炎症标记物 (MPO,NO,IL-1β,IL-6,INF-γ),NF-κB,JAK-1/STAT3信号传递,Ang II/Ang-(1-7) 轴,以及与亡相关的蛋白质 (Bax,Bcl-2,细胞染色体c,分裂的卡斯帕酶3).
主要成果:
- 佩尔治疗显著降低了血清尿素,肌素,尿酸和尿中的白蛋白/肌素比率.
- 通过降低NF-κB的调节和抑制JAK-1/STAT3酸化,PER通过降低MPO,NO,IL-1β,IL-6和INF-γ来减轻炎症.
- PER调节了Ang II/Ang-(1-7) 轴,通过改变Bax,Bcl-2,cytochrome c和分裂caspase 3水平来抑制Cd诱导的亡.
结论:
- 佩林多普利 (PER) 显示出显著的保护作用,防止 (Cd) 诱导的毒性.
- 通过NF-κB和JAK-1/STAT3通路抑制炎症,并调节Ang II/Ang-{1-7) 轴,PER发挥其保护作用.
- PER抑制了亡,突出了其作为重金属诱导损伤的治疗剂的潜力.
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