Dexmedetomidine alleviates intestinal ischemia/reperfusion injury by modulating intestinal neuron autophagy and mitochondrial homeostasis via Nupr1 regulation
- Mol Med. 2024 Nov 6;30(1):203. doi: 10.1186/s10020-024-00952-2.
- 1. Department of Surgery and Anesthesia, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 17, Yongwai Zhengjie, Donghu District, Nanchang, Jiangxi, 330006, China.
- 2. Department of Surgery and Anesthesia, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 17, Yongwai Zhengjie, Donghu District, Nanchang, Jiangxi, 330006, China. [email protected].
Intestinal ischemia/reperfusion injury (I/R) is a common yet challenging-to-treat condition, presenting a significant clinical challenge. This study aims to investigate the protective mechanisms of Dexmedetomidine (Dex) against I/R injury, with a particular focus on its role in regulating Autophagy activity in intestinal neurons and maintaining mitochondrial homeostasis. Experimental findings demonstrate that Dex can mitigate intestinal damage induced by I/R through the modulation of Autophagy activity and mitochondrial function in intestinal neurons by suppressing the expression of Nupr1. This discovery sheds light on a new molecular mechanism underlying the potential efficacy of Dex in treating intestinal I/R injury, offering valuable insights for clinical therapy.