Abstract | PURPOSE: 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.
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Authors | Meng-Xian Pan, Jun-Chun Tang, Rui Liu, Yu-Gong Feng, Qi Wan |
Journal | Chinese journal of traumatology = Zhonghua chuang shang za zhi
(Chin J Traumatol)
Vol. 21
Issue 4
Pg. 224-228
(Aug 2018)
ISSN: 1008-1275 [Print] China |
PMID | 30017543
(Publication Type: Journal Article)
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Copyright | Copyright © 2018 Daping Hospital and the Research Institute of Surgery of the Third Military Medical University. Production and hosting by Elsevier B.V. All rights reserved. |
Chemical References |
- Gper1 protein, rat
- Interleukin-1beta
- Receptors, G-Protein-Coupled
- Proto-Oncogene Proteins c-akt
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Topics |
- 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)
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