Skip to main content
. 2021 Mar 13;11(9):2859–2879. doi: 10.1016/j.apsb.2021.03.020

Figure 3.

Figure 3

FLZ treatment restores dopaminergic neuronal deficits via reducing neuroinflammation in the SN. (A) Representative captures of immunofluorescence in the SN of nuclei (DAPI, blue), total dopaminergic neurons (TH, green), and astrocytes (GFAP, red). (B)–(D) Numbers of TH+ cells (B), GFAP+ cells (C) and GFAP+/TH+ cells (activated astrocytes in SN) (D). (E) Representative captures of immunofluorescence in the SN of nuclei (DAPI, blue), total dopaminergic neurons (TH, green), and microglial cells (Iba-1, red). (F)–(H) Numbers of TH+ cells (F), Iba-1+ cells (G) and Iba-1+/TH+ cells (activated microglial cells in SN) (H). (I) Representative western blot brands of TH in SN. (J) The density analysis result of TH Western blot in SN. (K)–(L) mRNA expression of glial cell markers Gfap and Iba1, as well as (M)–(Q) neuroinflammatory markers (Cd3, Il1b, Il6, Cox 2, and Nos 2) in SN. In (B)–(D) and (F)–(H), n = 5 for each group. In (J), n = 4 for each group. In (K)–(Q), n = 3 for each group. Data are presented as mean ± SD. ##P < 0.01, ###P < 0.001 versus the Control group; ∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001 versus the Rotenone group.