脑周细胞的收缩和随后的死亡可能在缺血性中风期间闭塞动脉重新开放后的微血管无复流中发挥作用。哺乳动物雷帕霉素靶点 (mTOR) 抑制已被证明可以降低各种癌细胞系的运动性/收缩性，并减少中风时的神经元细胞死亡。然而，mTOR 抑制对缺血期间脑周细胞收缩和死亡的影响尚未得到研究。培养的周细胞在体外暴露于模拟缺血 12 小时后不到 1 小时即收缩，即细胞死亡前约 7 小时。雷帕霉素显着降低缺血时周细胞收缩率；然而，它在任何时间点都没有对周细胞活力产生显着影响。雷帕霉素似乎通过一种独立于细胞内钙变化的机制来减少周细胞收缩。使用大脑中动脉闭塞的小鼠模型，我们发现雷帕霉素显着增加了周细胞下方毛细血管的直径，并在再通后 30 分钟增加了开放毛细血管的数量。我们的研究结果表明，雷帕霉素可能是一种有用的辅助治疗剂，可减少周细胞收缩并改善中风后脑再灌注。© 2024。作者。

The contraction and subsequent death of brain pericytes may play a role in microvascular no-reflow following the reopening of an occluded artery during ischemic stroke. Mammalian target of rapamycin (mTOR) inhibition has been shown to reduce motility/contractility of various cancer cell lines and reduce neuronal cell death in stroke. However, the effects of mTOR inhibition on brain pericyte contraction and death during ischemia have not yet been investigated. Cultured pericytes exposed to simulated ischemia for 12 h in vitro contracted after less than 1 h, which was about 7 h prior to cell death. Rapamycin significantly reduced the rate of pericyte contraction during ischemia; however, it did not have a significant effect on pericyte viability at any time point. Rapamycin appeared to reduce pericyte contraction through a mechanism that is independent of changes in intracellular calcium. Using a mouse model of middle cerebral artery occlusion, we showed that rapamycin significantly increased the diameter of capillaries underneath pericytes and increased the number of open capillaries 30 min following recanalisation. Our findings suggest that rapamycin may be a useful adjuvant therapeutic to reduce pericyte contraction and improve cerebral reperfusion post-stroke.© 2024. The Author(s).