Fig. 4: COS produces anti-neuroinflammatory effects via inhibiting microglial Akt/mTOR/NF-κB pathway.

a–e Representative images (a) of Western blotting analysis and quantification showed that COS treatment prevented the increased phosphorylation protein expression of Akt (b), mTOR (c), S6 (d), NF-κB p65 (e) in BV2 cells induced by LPS exposure (n = 6 independent experiments per group). f–j Representative images (f) of Western blotting analysis and quantification showed that COS treatment prevented the increased phosphorylation protein expression of Akt (g), mTOR (h), S6 (i), NF-κB p65 (j) in DG induced by CRS (n = 6 mice per group). k–n Representative images (k) of Western blotting analysis and quantification showed that MHY1458 treatment (10 μM, 1 μL per side) blocked the decreased phosphorylation protein expression of mTOR (l), S6 (m), NF-κB p65 (n) in DG produced by COS treatment of CRS-exposed mice (n = 6 mice per group). o Representative images of Iba1 (top), three-dimensional (3D) reconstruction (middle) and cylinder (bottom) of microglia in DG (n = 12 cells from 3 mice per group). Scale bars, 10 μm. p–r Quantification showed that MHY1458 treatment blocked the decreased Iba1⁺ cell soma size (p) and the increased total process length (q) and number of intersections (r) of microglia in DG by COS treatment of CRS-exposed mice (n = 14 cells from 3 mice per group). Data are presented as mean ± SEM, ^*P < 0.05, ^**P < 0.01, ^***P < 0.001 by two-way ANOVA (b–e, g–j, l–n, p, q), repeated measures ANOVA (r) followed by Sidak’s post hoc test.