Background: The goal of this investigation was to examine the expression changes of H 2 S, IGF-1, and GH after TBI and to detect their roles after TBI.Methods: In this study, we rst collected cerebrospinal uid (CSF) and plasma from TBI patients at different times after injury and evaluated the concentrations of H 2 S, IGF-1, and GH. In vitro TBI conditions were stimulated by using HT22 hippocampal neurons and LPS-induced BV2 microglia cells. Models of TBI were established using controlled cortical impact (CCI) in vivo. CCK-8 assay, qRT-PCR and ELISA were used. Western blot was performed to assess the expression of CBS, CSE, IGF-1, and GHRH. Moreover, the recovery of TBI mice was evaluated for behavioral function by applying the modi ed Neurological Severity Score (mNSS), the Rotarod test, and the Morris water maze.Results: We discovered that serum H 2 S, CSF H 2 S, and serum IGF-1 concentrations were all adversely associated with the severity of the TBI, while the concentrations of IGF-1 and GH in CSF and GH in the serum were all positively related to TBI severity. Experiments in vitro and in vivo indicated that activated-BV2 cells enhanced the production of in ammatory cytokines and suppressed the cell viability of HT22 cells. In addition, treatment with NaHS, IGF-1, and GH alleviated the activation of BV2 cells. Furthermore, NaHS, IGF-1, and GH treatment alleviated motor function de cits after TBI.
Conclusion:This study gives novel information on the functions of H 2 S, IGF-1, and GH in TBI.