1. Academic Validation
  2. Colivelin Rescues Ischemic Neuron and Axons Involving JAK/STAT3 Signaling Pathway

Colivelin Rescues Ischemic Neuron and Axons Involving JAK/STAT3 Signaling Pathway

  • Neuroscience. 2019 Sep 15;416:198-206. doi: 10.1016/j.neuroscience.2019.07.020.
Hui Zhao 1 Yan Feng 2 Changjuan Wei 2 Yan Li 2 Hongshan Ma 3 Xuejiao Wang 3 Zhigang Cui 3 Wei-Na Jin 4 Fu-Dong Shi 5
Affiliations

Affiliations

  • 1 Shanxi Medical University, Taiyuan, China; Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
  • 2 Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
  • 3 Center for Neurological Diseases, The Third People's Hospital of Datong, Shanxi, China.
  • 4 China National Clinical Research Center for Neurological Diseases, Beijing Tiantan Hospital, Capital Medical University, Beijing, China; Advanced Innovation Center for Human Brain Protection, Capital Medical University, Beijing, China; Beijing Key Laboratory of Translational Medicine for Cerebrovascular Disease, Beijing, China; Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China.
  • 5 Shanxi Medical University, Taiyuan, China; China National Clinical Research Center for Neurological Diseases, Beijing Tiantan Hospital, Capital Medical University, Beijing, China; Advanced Innovation Center for Human Brain Protection, Capital Medical University, Beijing, China; Beijing Key Laboratory of Translational Medicine for Cerebrovascular Disease, Beijing, China; Department of Neurology, Tianjin Neurological Institute, Tianjin Medical University General Hospital, Tianjin, China. Electronic address: fshi66@gmail.com.
Abstract

Colivelin is a neuroprotective humanin family peptide with potent long-term capacity against Aβ deposition, neuronal Apoptosis, and synaptic plasticity deficits in neurodegenerative disease. We seek to investigate whether this effect of Colivelin also govern ischemic brain injury, and potential mechanism underlying the Colivelin-mediated action on ischemic neurons. We adopted 60 min induction of transient focal cerebral ischemia and reperfusion in mice. We found that relative to mice receiving vehicle, Colivelin administration decreased the neurological deficits and infarct lesion induced by brain ischemia. Colivelin inhibited axonal damage and neuronal death in brain tissue, which was associated with elevated anti-apoptotic gene expression in ischemic neurons as well as increased axonal growth up until two-weeks post-stroke. Moreover, Colivelin activated STAT3 signaling, which may partially contribute to its beneficial effect against neuronal death and axon growth. In conclusion, Colivelin induce anti-apoptotic genes up-regulation, and activate JAK/STAT3 signaling after ischemic stroke, which may contribute to its effects of rescuing ischemic neuronal death and axonal remodeling. This study may justify further works to examine Colivelin as a single or adjunct therapy in ischemic stroke.

Keywords

JAK/STAT3; axonal remodeling; colivelin; ischemic stroke; neuronal death.

Figures
Products