L-lactate preconditioning promotes plasticity-related proteins expression and reduces neurological deficits by potentiating GPR81 signaling in rat traumatic brain injury model

• Published in: Brain research 2020-11, Vol.1746, p.146945-146945, Article 146945
• Main Authors: Zhai, Xiuli, Li, Jinying, Li, Liya, Sun, Ye, Zhang, Xiaonan, Xue, Ying, lv, Jiaxin, Gao, Ye, Li, Shouxin, Yan, Wei, Yin, Shengming, Xiao, Zhaoyang
• Format: Article
• Language: English
• Subjects: GPR81; L-lactate; Neurological function recovery; Traumatic brain injury
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2020.146945

•L-lactate preconditioning reduces neurological deficits induced by TBI.•The protective roles of L-lactate preconditioning may be via GPR81 signaling pathway.•L-lactate preconditioning provides a potential therapeutic method for TBI. Currently, there is no efficacious pharmacological treatment for traumatic brain injury (TBI). Previous studies revealed that L-lactate preconditioning has shown rich neuroprotective effects against cerebral ischemia, and therefore has the potential to improve neurological outcomes after TBI. L-lactate played a neuroprotective role by activating GPR81 in diseases of the central nervous system (CNS) such as TBI and cerebral ischemia. In this study we investigated the effects of L-lactate preconditioning on TBI and explored the underlying mechanisms. In this study, the mNSS test revealed that L-lactate preconditioning alleviates the neurological deficit caused by TBI in rats. L-lactate preconditioning significantly increased the expression of GPR81, PSD95, GAP43, BDNF, and MCT2 24 h after TBI in the cortex and hippocampus compared with the sham group. Taken together, these data suggested that L-lactate preconditioning is an effective method with which to recover neurological function after TBI. This reveals the mechanism of L-lactate preconditioning on TBI and provides a potential therapeutic method for TBI in humans.