Purpose: To investigate the effects of estrogen G protein-coupled receptor 30 (GPR30) agonist G1 on hippocampal neuronal apoptosis and microglial polarization in rat traumatic brain injury (TBI). Methods: Male S...Purpose: To investigate the effects of estrogen G protein-coupled receptor 30 (GPR30) agonist G1 on hippocampal neuronal apoptosis and microglial polarization in rat traumatic brain injury (TBI). Methods: Male SD rats were randomly divided into sham group, TBI + vehicle group, TBI + G1 group. Experimental moderate TBI was induced using Feeney's weigh-drop method. GI (100μg/kg) or vehicle was intravenously injected from femoral vein at 30 rain post-injury. Rats were sacrificed at 24 h after injury for detection of neuronal apoptosis and microglia polarization. Neuronal apoptosis was assayed by immunofluorescent staining of active caspase-3. MI type microglia markers (iNOS and IL-113) and M2 type markers (Argl and IL-4) were examined by immunoblotting or ELLSA. Total protein level of Akt and phosphorylated Akt were assayed by immunoblotting. Results: G1 significantly reduced active caspase-3 positive neurons in hippocampus. Meanwhile G1 increased the ratio of Arg1/iNOS. IL-1β production was decreased but IL-4 was increased after G1 treatment. G1 treatment also increased the active form of Akt. Conclusions: GPR30 agonist GI inhibited neuronal apoptosis and favored microglia polarization to M2 type.展开更多
基金This work was supported by Natural Science Foundation of China (NSFC 81470599).
文摘Purpose: To investigate the effects of estrogen G protein-coupled receptor 30 (GPR30) agonist G1 on hippocampal neuronal apoptosis and microglial polarization in rat traumatic brain injury (TBI). Methods: Male SD rats were randomly divided into sham group, TBI + vehicle group, TBI + G1 group. Experimental moderate TBI was induced using Feeney's weigh-drop method. GI (100μg/kg) or vehicle was intravenously injected from femoral vein at 30 rain post-injury. Rats were sacrificed at 24 h after injury for detection of neuronal apoptosis and microglia polarization. Neuronal apoptosis was assayed by immunofluorescent staining of active caspase-3. MI type microglia markers (iNOS and IL-113) and M2 type markers (Argl and IL-4) were examined by immunoblotting or ELLSA. Total protein level of Akt and phosphorylated Akt were assayed by immunoblotting. Results: G1 significantly reduced active caspase-3 positive neurons in hippocampus. Meanwhile G1 increased the ratio of Arg1/iNOS. IL-1β production was decreased but IL-4 was increased after G1 treatment. G1 treatment also increased the active form of Akt. Conclusions: GPR30 agonist GI inhibited neuronal apoptosis and favored microglia polarization to M2 type.