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. 2021 Aug 11;9:693342. doi: 10.3389/fcell.2021.693342

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Copyright © 2021 Hu, Li, Wang, Chen, Qian and Dai.

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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Microglial Toll-like receptor 4 (TLR4) deficiency ameliorates the neuronal damage in the coculture system after subarachnoid hemorrhage (SAH). (A,B) The double immunofluorescence staining of triggering receptor expressed on myeloid cells 2 (TREM2)/CD68 was detected and quantified in microglial cells. (C) Double immunofluorescence staining showed the cell purity of primary neurons. (D–G) The MAP2 staining terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) labeling was quantified to reveal the regulation of microglial TLR4/TREM2 on primary neurons. These data are shown as mean ± SEM (*p<0.05, **p<0.01, ***p<0.001, ****p<0.001; A,C,D, scale bar = 25 μm; F, scale bar = 50 μm).