Tang Chaoliang, Hong Junmou, Hu Chengyun, Huang Chunxia, Gao Jie, Huang Jun, Wang Di, Geng Qingtian, Dong Yongfei
Department of Anesthesiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230001, China.
Department of Vascular Surgery, Zhongshan Hospital, Xiamen University, Xiamen, Fujian 361004, China.
Oxid Med Cell Longev. 2021 Mar 11;2021:6660193. doi: 10.1155/2021/6660193. eCollection 2021.
Palmatine (PAL), a natural isoquinoline alkaloid, possesses extensive biological and pharmaceutical activities, including antioxidative stress, anti-inflammatory, antitumor, neuroprotective, and gastroprotective activities. However, it is unknown whether PAL has a protective effect against ischemic stroke and cerebral ischemia/reperfusion (I/R) injury. In the present study, a transient middle cerebral artery occlusion (MCAO) mouse model was used to mimic ischemic stroke and cerebral I/R injury in mice. Our study demonstrated that PAL treatment ameliorated cerebral I/R injury by decreasing infarct volume, neurological scores, and brain water content. PAL administration attenuated oxidative stress, the inflammatory response, and neuronal apoptosis in mice after cerebral I/R injury. In addition, PAL treatment also decreases hypoxia and reperfusion- (H/R-) induced neuronal injury by reducing oxidative stress, the inflammatory response, and neuronal apoptosis. Moreover, the neuroprotective effects of PAL were associated with the activation of the AMP-activated protein kinase (AMPK)/nuclear factor E2-related factor 2 (Nrf2) pathway, and Nrf2 knockdown offsets PAL-mediated antioxidative stress and anti-inflammatory effects. Therefore, our results suggest that PAL may be a novel treatment strategy for ischemic stroke and cerebral I/R injury.
巴马汀（PAL）是一种天然异喹啉生物碱，具有广泛的生物学和药学活性，包括抗氧化应激、抗炎、抗肿瘤、神经保护和胃保护活性。然而，PAL对缺血性中风和脑缺血/再灌注（I/R）损伤是否具有保护作用尚不清楚。在本研究中，采用短暂性大脑中动脉闭塞（MCAO）小鼠模型来模拟小鼠的缺血性中风和脑I/R损伤。我们的研究表明，PAL治疗通过降低梗死体积、神经功能评分和脑含水量来改善脑I/R损伤。PAL给药减轻了脑I/R损伤后小鼠的氧化应激、炎症反应和神经元凋亡。此外，PAL治疗还通过减少氧化应激、炎症反应和神经元凋亡来减轻缺氧和再灌注（H/R）诱导的神经元损伤。此外，PAL的神经保护作用与AMP激活蛋白激酶（AMPK）/核因子E2相关因子2（Nrf2）通路的激活有关，Nrf2基因敲低可抵消PAL介导的抗氧化应激和抗炎作用。因此，我们的结果表明，PAL可能是缺血性中风和脑I/R损伤的一种新型治疗策略。
