1. Academic Validation
  2. Ebselen ameliorates renal ischemia-reperfusion injury via enhancing autophagy in rats

Ebselen ameliorates renal ischemia-reperfusion injury via enhancing autophagy in rats

  • Mol Cell Biochem. 2022 Jun;477(6):1873-1885. doi: 10.1007/s11010-022-04413-4.
Yikun Wu 1 Hua Shi 2 Yuangao Xu 3 Jun Pei 3 Shang Song 2 Wei Chen 3 Shuxiong Xu 4 5
Affiliations

Affiliations

  • 1 School of Medicine, Guizhou University, Guiyang, Guizhou, China.
  • 2 Department of Urology, Tongren City People's Hospital, Tongren, Guizhou, China.
  • 3 Department of Urology, Guizhou Provincial People's Hospital, Guiyang, Guizhou, China.
  • 4 School of Medicine, Guizhou University, Guiyang, Guizhou, China. [email protected].
  • 5 Department of Urology, Guizhou Provincial People's Hospital, Guiyang, Guizhou, China. [email protected].
Abstract

Renal ischemia-reperfusion (I/R) injury is one of the most common causes of chronic kidney disease (CKD). It brings unfavorable outcomes to the patients and leads to a considerable socioeconomic burden. The study of renal I/R injury is still one of the hot topics in the medical field. Ebselen is an organic selenide that attenuates I/R injury in various organs. However, its effect and related mechanism underlying renal I/R injury remains unclear. In this study, we established a rat model of renal I/R injury to study the preventive effect of ebselen on renal I/R injury and further explore the potential mechanism of its action. We found that ebselen pretreatment reduced renal dysfunction and tissue damage caused by renal I/R. In addition, ebselen enhanced Autophagy and inhibited oxidative stress. Additionally, ebselen pretreatment activated the nuclear factor erythroid 2-related factor 2 (Nrf2) signaling pathway. The protective effect of ebselen was suppressed by Autophagy Inhibitor wortmannin. In conclusion, ebselen could ameliorate renal I/R injury, probably by enhancing Autophagy, activating the Nrf2 signaling pathway, and reducing oxidative stress.

Keywords

Autophagy; Ebselen; Nrf2-signaling pathway; Oxidative stress; Renal ischemia–reperfusion injury.

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