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. 2020 Feb 25;11:128. doi: 10.3389/fphar.2020.00128

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Copyright © 2020 Zhao, Feng, Li, Sha, Wang, Yang, Cui and Fan

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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The potential protective mechanisms of DEX in reducing oxidative stress and apoptosis in LPS-induced AKI. LPS could hold back the formation of autophagosome via activating the PI3K/AKT/mTOR pathway, inducing the accumulation of damaged mitochondria. Then ROS and Cyt C released from damaged mitochondria could induce oxidative stress and apoptosis. DEX could inhibit the PI3K/AKT/mTOR pathway to enhance autophagy by α₂-AR, reducing oxidative stress and apoptosis. 3-MA could inhibit the effect of DEX on autophagy.