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. 2022 Jun 13;13:903565. doi: 10.3389/fneur.2022.903565

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Copyright © 2022 Yu, Zheng, Cheng, Shao, Zhuge and Jin.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Potential mechanisms underlying neuroprotection of metformin, rapamycin, and NMN after BCCAO in rats. In chronic cerebral hypoperfusion (CCH) rats, activated microglia (M1) increase and destroy white matter integrity by releasing pro-inflammatory factors (like IL-6, IL-1β) and inhibiting oligodendrogenesis and myelination via microglial phagocytosis. Metformin and NMN could activate AMP-activated protein kinase (AMPK) and Sirtuin 1 (SIRT1), respectively. Rapamycin inhibits mTOR to increase M2 microglial polarization. AMPK and SIRT1 could also inhibit M1 polarization by decreasing the expression of NF-κB, as well as promoting M2 polarization. The activation of AMPK and the inhibition of mTOR could promote phagocytosis via the phosphorylation of ULK1, while SIRT1 could promote phagocytosis through deacetylation of transcription factor EB (TFEB). There is a complex interplay among AMPK, mTOR, and SIRT1.