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.
