Yu Sicong, Liao Jian, Lin Xuezheng, Luo Yu, Lu Guangtao
Department of Anesthesiology, Taizhou Central Hospital (Taizhou University Hospital), Taizhou, China.
Department of Nephrology, Jiaxing Hospital of Traditional Chinese Medicine, Jiaxing, China.
Front Cell Neurosci. 2023 Oct 25;17:1274727. doi: 10.3389/fncel.2023.1274727. eCollection 2023.
Neurological disorders are the leading cause of disability and death globally. Currently, there is a significant concern about the therapeutic strategies that can offer reliable and cost-effective treatment for neurological diseases. Propofol is a widely used general intravenous anesthetic in the clinic. Emerging studies demonstrate that propofol exerts neuroprotective effects on neurological diseases and disorders, while its underlying pathogenic mechanism is not well understood. Autophagy, an important process of cell turnover in eukaryotes, has been suggested to involve in the neuroprotective properties developed by propofol. In this narrative review, we summarized the current evidence on the roles of autophagy in propofol-associated neurological diseases. This study highlighted the effect of propofol on the nervous system and the crucial roles of autophagy. According to the 21 included studies, we found that propofol was a double-edged sword for neurological disorders. Several eligible studies reported that propofol caused neuronal cell damage by regulating autophagy, leading to cognitive dysfunction and other neurological diseases, especially high concentration and dose of propofol. However, some of them have shown that in the model of existing nervous system diseases (e.g., cerebral ischemia-reperfusion injury, electroconvulsive therapy injury, cobalt chloride-induced injury, TNF-α-induced injury, and sleep deprivation-induced injury), propofol might play a neuroprotective role by regulating autophagy, thus improving the degree of nerve damage. Autophagy plays a pivotal role in the neurological system by regulating oxidative stress, inflammatory response, calcium release, and other mechanisms, which may be associated with the interaction of a variety of related proteins and signal cascades. With extensive in-depth research in the future, the autophagic mechanism mediated by propofol will be fully understood, which may facilitate the feasibility of propofol in the prevention and treatment of neurological disorders.
神经疾病是全球致残和致死的主要原因。目前,人们对能够为神经疾病提供可靠且具成本效益治疗的策略极为关注。丙泊酚是临床上广泛使用的全身静脉麻醉剂。新出现的研究表明,丙泊酚对神经疾病和紊乱具有神经保护作用,但其潜在的致病机制尚不完全清楚。自噬是真核生物中细胞更新的一个重要过程,已被认为与丙泊酚产生的神经保护特性有关。在这篇叙述性综述中,我们总结了目前关于自噬在丙泊酚相关神经疾病中作用的证据。本研究强调了丙泊酚对神经系统的影响以及自噬的关键作用。根据纳入的21项研究,我们发现丙泊酚对神经疾病是一把双刃剑。几项符合条件的研究报告称,丙泊酚通过调节自噬导致神经元细胞损伤,进而引发认知功能障碍和其他神经疾病,尤其是高浓度和高剂量的丙泊酚。然而,其中一些研究表明,在现有的神经系统疾病模型(如脑缺血再灌注损伤、电惊厥治疗损伤、氯化钴诱导的损伤、肿瘤坏死因子-α诱导的损伤和睡眠剥夺诱导的损伤)中,丙泊酚可能通过调节自噬发挥神经保护作用,从而改善神经损伤程度。自噬通过调节氧化应激、炎症反应、钙释放等机制在神经系统中发挥关键作用,这可能与多种相关蛋白和信号级联的相互作用有关。随着未来广泛深入的研究,丙泊酚介导的自噬机制将被充分了解,这可能会促进丙泊酚在预防和治疗神经疾病方面的可行性。