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雌激素受体GPR30激动剂G1对创伤性脑损伤大鼠神经元凋亡和小胶质细胞极化的影响

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

作者信息

Pan Meng-Xian, Tang Jun-Chun, Liu Rui, Feng Yu-Gong, Wan Qi

机构信息

Department of Physiology, Collaborative Innovation Center for Brain Science, School of Basic Medical Sciences, Wuhan University School of Medicine, Wuhan 430071, China.

Institute of Neuroregeneration & Neurorehabilitation, Department of Neurosurgery, Qingdao University, Qingdao 266071, China.

出版信息

Chin J Traumatol. 2018 Aug;21(4):224-228. doi: 10.1016/j.cjtee.2018.04.003. Epub 2018 May 18.

DOI:10.1016/j.cjtee.2018.04.003
PMID:30017543
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6085194/
Abstract

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. 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.

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 G1 inhibited neuronal apoptosis and favored microglia polarization to M2 type.

摘要

目的

探讨雌激素G蛋白偶联受体30（GPR30）激动剂G1对大鼠创伤性脑损伤（TBI）后海马神经元凋亡及小胶质细胞极化的影响。

方法

将雄性SD大鼠随机分为假手术组、TBI+溶剂组、TBI+G1组。采用Feeney自由落体法诱导实验性中度TBI。伤后30分钟经股静脉静脉注射G1（100μg/kg）或溶剂。伤后24小时处死大鼠，检测神经元凋亡及小胶质细胞极化情况。通过活性半胱天冬酶-3免疫荧光染色检测神经元凋亡。通过免疫印迹法或酶联免疫吸附测定法检测M1型小胶质细胞标志物（诱导型一氧化氮合酶和白细胞介素-1β）和M2型标志物（精氨酸酶1和白细胞介素-4）。通过免疫印迹法检测Akt和磷酸化Akt的总蛋白水平。

结果

G1显著减少海马中活性半胱天冬酶-3阳性神经元。同时，G1增加了精氨酸酶1/诱导型一氧化氮合酶的比值。G1处理后白细胞介素-1β的产生减少，但白细胞介素-4增加。G1处理还增加了Akt的活性形式。

结论

GPR30激动剂G1抑制神经元凋亡，并有利于小胶质细胞向M2型极化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb2b/6085194/4bacbe977539/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb2b/6085194/00ccf1526e66/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb2b/6085194/6abdff97a792/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb2b/6085194/4bacbe977539/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb2b/6085194/00ccf1526e66/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb2b/6085194/6abdff97a792/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cb2b/6085194/4bacbe977539/gr3.jpg

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