2-BFI attenuates ischemic injury by modulating mTOR signaling and neuroinflammation in rats. (17th April 2021)

• Record Type: Journal Article
• Authors: Cheng, Yifan; Zhang, Wanli; Cao, Wen; Shao, Mengmeng; Lin, Yuanshao; Shao, Bei; Yu, Huan; Deng, Binbin
• Is Part Of: Neuroscience letters. Volume 750(2021)
• Publication Date: 2021-04-17
• Subjects: 2-BFI 2-(2-Benzofuranyl)-2-Imidazoline -- mTOR mammalian target of rapamycin -- dMCAO distal middle cerebral artery occlusion; Ischemic stroke -- 2-BFI -- mTOR -- Neuroinflammation -- Neuroprotection; Neurology -- Periodicals; Neurology -- Periodicals; Research -- Periodicals; Neurologie -- Périodiques; Neuroanatomie -- Périodiques; Neuropharmacologie -- Périodiques; Neurophysiologie -- Périodiques; Neurology; Periodicals; Electronic journals; 617.48
• DOI: 10.1016/j.neulet.2021.135766
• Languages: English
• ISSNs: 0304-3940

Abstract

Highlights: There is lack of effective treatment and prevention for stroke. Modulation of mTOR signaling has been considered as a novel therapeutic strategy for stroke. 2-BFI might be an excellent candidate as a therapeutic drug for stroke. 2-BFI may attenuates ischemic injury by modulating mTOR signaling and neuroinflammation in rats. 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.