Effects of estrogen receptor GPR30 agonist G1 on neuronal apoptosis and microglia polarization in traumatic brain injury rats.

Meng-xian Pan; Jun-chun Tang; Rui Liu; Yu-gong Feng; Qi Wan

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Effects of estrogen receptor GPR30 agonist G1 on neuronal apoptosis and microglia polarization in traumatic brain injury rats.

Author: Meng-Xian PAN ¹ ; Jun-Chun TANG ¹ ; Rui LIU ¹ ; Yu-Gong FENG ² ; Qi WAN ^{3
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Author Information

1. Department of Physiology, Collaborative Innovation Center for Brain Science, School of Basic Medical Sciences, Wuhan University School of Medicine, Wuhan 430071, China.
2. Institute of Neuroregeneration & Neurorehabilitation, Department of Neurosurgery, Qingdao University, Qingdao 266071, China.
3. Department of Physiology, Collaborative Innovation Center for Brain Science, School of Basic Medical Sciences, Wuhan University School of Medicine, Wuhan 430071, China
4. Institute of Neuroregeneration & Neurorehabilitation, Department of Neurosurgery, Qingdao University, Qingdao 266071, China. Electronic address: qwanwh@hotmail.com.
Publication Type:Journal Article
Keywords: GPR30; Microglia; Neuron; Traumatic brain injury
MeSH: Animals; Apoptosis; drug effects; Brain Injuries, Traumatic; drug therapy; pathology; Cell Polarity; Hippocampus; drug effects; Interleukin-1beta; biosynthesis; Male; Microglia; drug effects; Neurons; drug effects; Proto-Oncogene Proteins c-akt; metabolism; Rats; Rats, Sprague-Dawley; Receptors, G-Protein-Coupled; agonists
From: Chinese Journal of Traumatology 2018;21(4):224-228
CountryChina
Language:English
Abstract:
PURPOSETo 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).
METHODSMale 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. G1 (100μg/kg) or vehicle was intravenously injected from femoral vein at 30 min 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. M1 type microglia markers (iNOS and IL-1β) and M2 type markers (Arg1 and IL-4) were examined by immunoblotting or ELISA. Total protein level of Akt and phosphorylated Akt were assayed by immunoblotting.
RESULTSG1 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.
CONCLUSIONSGPR30 agonist G1 inhibited neuronal apoptosis and favored microglia polarization to M2 type.