1. 2-BFI attenuates ischemic injury by modulating mTOR signaling and neuroinflammation in rats.
- Author
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Cheng Y, Zhang W, Cao W, Shao M, Lin Y, Shao B, Yu H, and Deng B
- Subjects
- Affinity Labels pharmacology, Animals, Anti-Inflammatory Agents pharmacology, Benzofurans pharmacology, Imidazoles pharmacology, Infarction, Middle Cerebral Artery metabolism, Male, Rats, Rats, Sprague-Dawley, Signal Transduction, Affinity Labels therapeutic use, Anti-Inflammatory Agents therapeutic use, Benzofurans therapeutic use, Imidazoles therapeutic use, Infarction, Middle Cerebral Artery drug therapy, TOR Serine-Threonine Kinases metabolism
- Abstract
Ischemic stroke is one of the major diseases that cause mortality and morbidity of human beings, but there is still lack of effective treatment and prevention. We found that 2-(2-Benzofuranyl)-2-Imidazoline (2-BFI) is potently protective against stroke and acute inflammatory immune disease. Moreover, the mammalian target of rapamycin (mTOR) signaling contributes effectively to the modulation of post-stroke neuroinflammatory response. However, whether the protection of 2-BFI against ischemic injury is through mTOR-mediated neuroinflammatory response remains unestablished. Here, we used 2-BFI to treat ischemic rats induced by distal middle cerebral artery occlusion (dMCAO). We found that 2-BFI administration after dMCAO improved the neurological deficits and decreased the infarct volume. 2-BFI reduced phosphorylation of mTOR and p70S6, increased IL-10 and TGF-β, and decreased IFN-γ levels in ischemic rats. Our results demonstrated that 2-BFI attenuates ischemic injury by inhibiting the activation of mTOR signaling and modulating neuroinflammation after stroke in rats., (Copyright © 2021 Elsevier B.V. All rights reserved.)
- Published
- 2021
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