Department of Anesthesiology, Cangzhou Central Hospital, Teaching Hospital of Tianjin Medical University, Cangzhou 061000, Hebei, China.
Department of Anesthesiology, Cangzhou Central Hospital, Teaching Hospital of Tianjin Medical University, Cangzhou 061000, Hebei, China.
Gene. 2020 May 30;741:144562. doi: 10.1016/j.gene.2020.144562. Epub 2020 Mar 10.
Renal Ischemia/Reperfusion (rI/R)-induced acute lung injury (ALI) is a major problem in rI/R. The objective of the current study was to explore the defensive roles of propofol (Pro), an intravenous anesthetic, on rI/R-induced ALI through mitogen-activated protein kinase (MAPK) signaling. Rats were divided into Sham, Pro (10 mg/kg), rI/R, rI/R + Pro (5 mg/kg), and rI/R + Pro (10 mg/kg) groups. Rats were treated with Pro at 1 h after rI/R treatment. Serum and lung tissues at 24 h after rI/R were collected to evaluate morphological changes and the expression of myeloperoxidase (MPO), inflammatory cytokines, and crucial proteins in the MAPK pathway. Pro attenuated the production of mediators, resulting in reduced levels of autophagy and apoptosis by restricting the MAPK pathway in rI/R-induced ALI model. Pro represses rI/R-induced pulmonary autophagy and apoptosis by decreasing the production of inflammatory molecules, and the effects of Pro are involved in the inhibition of the MAPK pathway.
肾缺血/再灌注（rI/R）引起的急性肺损伤（ALI）是 rI/R 的一个主要问题。本研究的目的是通过丝裂原活化蛋白激酶（MAPK）信号通路探讨异丙酚（Pro），一种静脉麻醉剂，对 rI/R 诱导的 ALI 的保护作用。大鼠分为假手术组、Pro（10mg/kg）组、rI/R 组、rI/R+Pro（5mg/kg）组和 rI/R+Pro（10mg/kg）组。rI/R 治疗后 1 小时给予 Pro 治疗。rI/R 后 24 小时收集血清和肺组织，评估形态变化以及髓过氧化物酶（MPO）、炎症细胞因子和 MAPK 通路中关键蛋白的表达。Pro 通过限制 MAPK 通路减轻了 rI/R 诱导的 ALI 模型中介质的产生，从而减少了自噬和细胞凋亡的发生。Pro 通过减少炎症分子的产生抑制 rI/R 诱导的肺自噬和凋亡，Pro 的作用涉及 MAPK 通路的抑制。
