In injury. (C) ARKO mice show afterafter TBI.The quantitative information of GFAP level at four hat 4 h following brain injury. (C) ARKO mice show TBI-induced GFAP expression enhancement compared 24 h just after TBI. (D) TBI. (D) QuantiTBI-induced GFAP expression enhancement compared with WTwith WT 24 h after Quantitative information tative data of GFAPhlevel at 24 hTBI. All information are presented as the mean standard typical erof GFAP level at 24 following following TBI. All data are presented as the imply error. NS, no ror. NS, no significant difference; p 0.01, and p 0.001; n = 3 in each group. important distinction; p 0.01, and p 0.001; n = 3 in every group.Molecules 2021, 26, 6250 Molecules 2021, 26, x FOR PEER REVIEW5 of 16 five ofFigure 3. Androgen receptor knockout increases the TBI-induced GFAP expression about thethe Figure 3. Androgen receptor knockout increases the TBI-induced GFAP expression about cortical injury site. (A) Illustrations from the regions of interest (white areas) the mice brain after TBI cortical injury web page. (A) Illustrations from the regions of interest (white areas) ofof the mice brain soon after TBI are shown in left panel. WT ARKO mice were performed with TBI or sham, after which stained are shown in left panel. WT and and ARKO mice had been performed with TBI or sham, after which stained with immunofluorescence of GFAP. The GFAP cells have been indicated by white white arwith immunofluorescence of GFAP. The GFAP positive positive cells had been indicated byarrowhead. rowhead. ARKO mice showed the cells of GFAP of GFAP expression. Blue colour, DAPI (four,6ARKO mice showed the increasingincreasing cellsexpression. Blue color, DAPI (four ,6-diamidino-2diamidino-2-phenylindole); red color, GFAP. (Photos: x200 magnification from the ipsilateral as well as the phenylindole); red colour, GFAP. (Photos: x200 magnification with the ipsilateral and also the contralateral contralateral IL-4 Protein supplier hemispheres; scale bar = 100 m) (B) The intensity of GFAP immunoreactive level hemispheres; scale bar = 100 ) (B) The intensity of GFAP immunoreactive level with normalized with normalized intensity fluorescence unit in the four experimental groups is presented. (C) The intensity fluorescence positive cells counterstained with DAPI 3-Chloro-5-hydroxybenzoic acid Protocol inside the four experimental groups is percentage of GFAP unit within the four experimental groups is presented. (C) The percentage of GFAP constructive cells counterstainedof GFAP at the corticalexperimental groups is presented. The expression presented. The expression with DAPI in the four injury website was calculated from six diverse of GFAP levels.corticalwild-type sham; WT-T, wild-type with TBI; ARKO-S, ARKO sham; ARKO-T, bregma at the WT-S, injury web-site was calculated from six distinct bregma levels. WT-S, wild-type ARKO with wild-type with presented as the mean normal error. NS, no substantial difference; sham; WT-T, TBI. All data areTBI; ARKO-S, ARKO sham; ARKO-T, ARKO with TBI. All information are p 0.05, and p 0.001; n = 7 in every NS, no presented as the mean typical error. group. substantial distinction; p 0.05, and p 0.001; n = 7 in each group.2.three. Effects of Androgen Receptor Knockout on Beclin-1 Expression in Mice Following TBI 2.3. Effects of Androgen Receptor Knockout on Beclin-1 Expression in Mice following TBI Since autophagy plays a outstanding function in brain injury, we evaluated whether or not the Because receptor is involved in TBI-associated brain injury and autophagy. Figure 4A androgen autophagy plays a outstanding function in brain injury, we evaluated irrespective of whether the androgen.