Palmatine Protects against Cerebral Ischemia/Reperfusion Injury by Activation of the AMPK/Nrf2 Pathway

  • Oxid Med Cell Longev. 2021 Mar 11:2021:6660193. doi: 10.1155/2021/6660193.
Chaoliang Tang  1 ,  Junmou Hong  2 ,  Chengyun Hu  1 ,  Chunxia Huang  3 ,  Jie Gao  4 ,  Jun Huang  5 ,  Di Wang  3 ,  Qingtian Geng  1 ,  Yongfei Dong  6
Affiliations
  • 1. 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.
  • 2. Department of Vascular Surgery, Zhongshan Hospital, Xiamen University, Xiamen, Fujian 361004, China.
  • 3. Department of Anesthesiology, The Second Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230601, China.
  • 4. Department of Anesthesiology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, China.
  • 5. Department of Anesthesiology, The People's Hospital of Chizhou, Chizhou, Anhui 247000, China.
  • 6. Department of Neurosurgery, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui 230001, China.
PMID: 33777318 DOI: 10.1155/2021/6660193
Abstract

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.

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