Dataset Information

LncRNA-1810034E14Rik reduces microglia activation in experimental ischemic stroke.

ABSTRACT:

Background

Activation of microglial cells plays an important role in neuroinflammation after ischemic stroke. Inhibiting the activation of microglial cells has been suggested as a potential therapeutic approach in the treatment of ischemic stroke.

Methods

Oxygen-glucose deprivation in primary microglial cells and transient middle cerebral artery occlusion (MCAO) in C57BL/6 mice were used as the in vitro and in vivo ischemic stroke models. Microarray analysis was performed to investigate the overall impact of long non-coding RNAs (lncRNAs) on the inflammation status of microglial cells. RT-qPCR was used to evaluate the lncRNA levels and mRNA levels of cytokines and microglial cell markers. ELISA was taken to measure the level of cytokines. Immunofluorescence was used to observe the activation of microglial cells. Western blotting was performed to test the p65 phosphorylation.

Results

In this study, we showed that LncRNA-1810034E14Rik was significantly decreased in LPS-treated or oxygen-glucose deprivation-induced microglial cells. Overexpression of 1810034E14Rik decreased the infarct volume and alleviated brain damage in MCAO mice. 1810034E14Rik overexpression reduced the expression of inflammatory cytokines not only in ischemic stroke mice but also in oxygen-glucose deprivation-induced microglial cells. Moreover, 1810034E14Rik overexpression could suppress the activation of microglial cells and inhibit the phosphorylation of p65.

Conclusions

LncRNA-1810034E14Rik plays an anti-inflammatory role in ischemic stroke and regulates p65 phosphorylation, making it a potential target for stroke treatment.

SUBMITTER: Zhang X

PROVIDER: S-EPMC6452518 | biostudies-literature | 2019 Apr

REPOSITORIES: biostudies-literature

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Publications

LncRNA-1810034E14Rik reduces microglia activation in experimental ischemic stroke.

Zhang Xi X Zhu Xiao-Lei XL Ji Bi-Ying BY Cao Xiang X Yu Lin-Jie LJ Zhang Yan Y Bao Xin-Yu XY Xu Yun Y Jin Jia-Li JL

Journal of neuroinflammation 20190408 1

<h4>Background</h4>Activation of microglial cells plays an important role in neuroinflammation after ischemic stroke. Inhibiting the activation of microglial cells has been suggested as a potential therapeutic approach in the treatment of ischemic stroke.<h4>Methods</h4>Oxygen-glucose deprivation in primary microglial cells and transient middle cerebral artery occlusion (MCAO) in C57BL/6 mice were used as the in vitro and in vivo ischemic stroke models. Microarray analysis was performed to inves ...[more]

PMID: 30961627

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Project description:BACKGROUND:Ischemic stroke is the second leading cause of death globally. The narrow time window for administering effective thrombolytic therapy motivates the search for alternative prevention strategies. Microglia and astrocyte activation-mediated inflammation play a pivotal role in ischemic stroke injury. Cottonseed oil (CSO) has been shown to exert anti-inflammatory effects against peripheral tissue injury, although CSO is mostly used as a solvent for lipid-soluble drugs. However, the role of CSO in neuroprotection against stroke has not been previously reported. METHODS:We treated adult male rats with CSO (1.3?ml/kg, subcutaneous injection, once every other day for 3?weeks) and then constructed a middle cerebral artery occlusion (MCAO) model followed by 24?h of reperfusion. Then, we measured the neurological scores, infarction volume, neuronal injury, and brain edema; we also measured the levels of pro-inflammatory cytokines (IL-1?, IL-6, TNF-?), degree of microglial and astrocytic activation, protein expression levels of Toll-like receptor 4 (TLR4), nuclear factor kappa B (NF-?B), C3d and S100A10, and the presence of A1 type astrocytes and A2 type astrocytes. RESULTS:We found that CSO treatment significantly improved the neurological deficit, reduced infarction volume, and alleviated neuronal injuries, blood-brain barrier (BBB) disruption, and brain edema. Additionally, CSO treatment significantly reduced microglial and astrocytic activation, inhibited TLR4 and NF-?B protein expression, and reduced the release of IL-1?, IL-6, and TNF-?. Finally, CSO treatment significantly decreased the number of C3d/glial fibrillary acidic protein (GFAP)-positive cells and C3d protein expression, and increased the number of S100A10/GFAP-positive cells and S100A10 protein expression. CONCLUSION:Our results first found that CSO treatment alleviated ischemic stroke injury by reducing microglial and astrocytic activation and inflammation, which was related to the inhibition of TLR4/NF-?B pathway and the reduction of A1 phenotype neurotoxic astrocyte activation, suggesting that CSO could be a new strategy in the prevention of ischemic stroke.

Dataset Information

LncRNA-1810034E14Rik reduces microglia activation in experimental ischemic stroke.

Background

Methods

Results

Conclusions

Publications

LncRNA-1810034E14Rik reduces microglia activation in experimental ischemic stroke.

Similar Datasets

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