L-glutamine protects mouse brain from ischemic injury via up-regulating heat shock protein 70.

Luo, Long-Long; Li, Yong-Fang; Shan, Hui-Min; Wang, Li-Ping; Yuan, Fang; Ma, Yuan-Yuan; Li, Wan-Lu; He, Ting-Ting; Wang, Yu-Yang; Qu, Mei-Jie; Liang, Huai-Bin; Zhang, Zhi-Jun; Yang, Guo-Yuan; Tang, Yao-Hui; Wang, Yong-Ting

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.