Department of Surgery and Anesthesia, The First Affiliated Hospital, Jiangxi Medical College, Nanchang University, No. 17, Yongwai Zhengjie, Donghu District, Nanchang, Jiangxi, 330006, China.
Mol Med. 2024 Nov 6;30(1):203. doi: 10.1186/s10020-024-00952-2.
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.
肠缺血/再灌注损伤（I/R）是一种常见但治疗困难的疾病，具有很大的临床挑战性。本研究旨在探讨右美托咪定（Dex）对 I/R 损伤的保护机制，特别关注其在调节肠神经元自噬活性和维持线粒体动态平衡中的作用。实验结果表明，Dex 通过抑制 Nupr1 的表达来调节肠神经元的自噬活性和线粒体功能，从而减轻 I/R 引起的肠道损伤。这一发现揭示了 Dex 治疗肠道 I/R 损伤的潜在疗效的新分子机制，为临床治疗提供了有价值的见解。
