L-glutamine protects mouse brain from ischemic injury via up-regulating heat shock protein 70
- CNS Neurosci Ther. 2019 Sep;25(9):1030-1041. doi: 10.1111/cns.13184.
- 1. Shanghai Jiao Tong Affiliated Sixth People's Hospital, Neuroscience and Neuroengineering Research Center, Med-X Research Institute and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
- 2. Department of Neurology, School of Medicine, Ruijin Hospital, Shanghai Jiao Tong University, Shanghai, China.
- 3. Department of Rehabilitation Medicine, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
- 4. Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao University, Qingdao, China.
Introduction: L-glutamine is an antioxidant that plays a role in a variety of biochemical processes. Given that oxidative stress is a key component of stroke pathology, the potential of L-glutamine in the treatment of ischemic stroke is worth exploring.
Aims: In this study, we investigated the effect and mechanisms of action of L-glutamine after cerebral ischemic injury.
Results: L-glutamine reduced brain infarct volume and promoted neurobehavioral recovery in mice. L-glutamine administration increased the expression of heat-shock protein 70 (HSP70) in astrocytes and endothelial cells. Such effects were abolished by the coadministration of Apoptozole, an inhibitor of the ATPase activity of HSP70. L-glutamine also reduced oxidative stress and neuronal Apoptosis, and increased the level of superoxide dismutase, glutathione, and brain-derived neurotrophic factor. Cotreatment with Apoptozole abolished these effects. Cell Culture study further revealed that the conditioned medium from astrocytes cultured with L-glutamine reduced the Apoptosis of neurons after oxygen-glucose deprivation.
Conclusion: L-glutamine attenuated ischemic brain injury and promoted functional recovery via HSP70, suggesting its potential in ischemic stroke therapy.
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Research Areas: Neurological Disease; Metabolic Disease; Inflammation/Immunology; Cardiovascular Disease