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. 2019 Jan 7;12:516. doi: 10.3389/fncel.2018.00516

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Copyright © 2019 Fan, Song, Wang, Li, Yang and Yu.

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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Knocking-down of IL-1β in vmPFC reduced apoptosis-related factors produced by CUMS exposure. (A) Phosphorylation levels of p38 MAPK in the vmPFC infected with the AAV-IL-1β RNAi virus. (B) RT-PCR assays of expression levels of Bcl-2, Bak, Caspase 3 and Caspase 9 in vmPFC neurons infected with the AAV-IL-1β RNAi construct. (C) ELISA assays of expression levels of Bcl-2, Bak, Caspase 3 and Caspase 9 in vmPFC neurons infected with the AAV-IL-1β RNAi construct. N = 6/group. ^∗P < 0.05, ^∗∗P < 0.01, ^∗∗∗P < 0.001 Stressed rats vs. WT rats. #P < 0.05, ##P < 0.01, ###P < 0.001 S+AAV-IL-1β RNAi vs. Stressed rats.