Zhang Li-Na, Zhang Xian-Wei, Li Chang-Qing, Guo Jing, Chen Yong-Ping, Chen Sheng-Li
Department of Neurology, Chongqing University Three Gorges Hospital, Chongqing, 404000, People's Republic of China.
Department of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, 400010, People's Republic of China.
Neuropsychiatr Dis Treat. 2021 Mar 25;17:905-913. doi: 10.2147/NDT.S300535. eCollection 2021.
Cumulative evidence suggests that neuronal death including autophagy, apoptosis, and necrosis is closely related to the occurrence and development of cerebral ischemia-reperfusion (I/R) injury. Moreover, vagal nerve stimulation (VNS) is involved in many different neuroprotective and neuroplasticity pathways. Thus, VNS may be a novel approach for treating various neurodegenerative diseases. The present study aims to determine whether VNS protects against cerebral I/R injury in rats by inhibiting autophagy and apoptosis.
Cerebral I/R injury is induced by middle cerebral artery occlusion (MCAO) and VNS is carried out. Infarct volume, neurological deficit, autophagy, and apoptosis are examined 24 h after reperfusion.
Vagal nerve stimulation decreases infarct volume and suppresses neurological deficit. Moreover, obvious autophagy and apoptosis are detected in rats that have undergone I/R, and VNS inhibits autophagy and apoptosis.
Vagal nerve stimulation exerts neuroprotective effects following I/R injury by inhibiting autophagy and apoptosis.
越来越多的证据表明，包括自噬、凋亡和坏死在内的神经元死亡与脑缺血再灌注（I/R）损伤的发生和发展密切相关。此外，迷走神经刺激（VNS）参与多种不同的神经保护和神经可塑性途径。因此，VNS可能是治疗各种神经退行性疾病的一种新方法。本研究旨在确定VNS是否通过抑制自噬和凋亡来保护大鼠免受脑I/R损伤。
通过大脑中动脉闭塞（MCAO）诱导脑I/R损伤并进行VNS。再灌注24小时后检查梗死体积、神经功能缺损、自噬和凋亡情况。
迷走神经刺激可减小梗死体积并抑制神经功能缺损。此外，在经历I/R的大鼠中检测到明显的自噬和凋亡，而VNS可抑制自噬和凋亡。
迷走神经刺激通过抑制自噬和凋亡对I/R损伤发挥神经保护作用。
