Figure 4.

Sal alleviated neuronal injury and downregulated Aβ, P-Tau in Aβ1-42 and D-gal/AlCl₃-induced AD mice. (A) Representative photomicrograph of Nissl staining in the CA1, CA3, and DG regions of the hippocampus of the Aβ1-42 and D-gal/AlCl₃-treated group. Neuronal damage increased after administration of Aβ1-42 and D-gal/AlCl₃. Sal or DNP treatment significantly decreased neuronal injury. Nissl staining results are shown by arrows. Scale bar = 25 μm, the magnification of merge is 400 × (n = 3). (B) Aβ1–42 enzyme-linked immunosorbent assay kits were performed to measure the expression of Aβ1-42 in the hippocampus of AD mice (n = 4). (C) Brain AD biomarkers (Aβ1-42, Tau, and P-Tau) were determined by Western blotting. Aβ1-42 values were normalized using β-actin, and P-Tau values were normalized using Tau. Data are reported as Mean ± SEM (n = 3). ^##P < 0.01, ^###P < 0.001 vs. control group, ^*P < 0.05, ^**P < 0.01, ^***P < 0.001 vs. Aβ1-42 and D-gal/AlCl₃ group.