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. 2019 Mar 29;10:297. doi: 10.3389/fphar.2019.00297

FIGURE 4.

FIGURE 4

Melatonin induces neuroprotection via PI3K/AKT/GSK-3β/CRMP2 pathway. (A) Western blot analysis of γ–enolase, p-PI3K, p-Akt, Akt, p-GSK-3β, GSK-3β, CRMP2, p-CRMP2 from cortical, and striatal tissues (n = 7 rats/group). The bands were quantified using ImageJ, analyzed by graph-pad prism-5 software. β-actin was used as control. Densitometric analysis was expressed in arbitrary units as the mean ± SEM for the indicated proteins. (B) Immunofluorescence reactivity of γ-enolase and p-PI3K; (n = 7 rats/group). The above data is representation of 3 numbers of experiments. Scale bar = 100 μm and magnification 40×(A) γ-enolase (B) p-PI3K show cytoplasmic localization and was visualized by TRITC and FITC. (C) Double immunofluorescence of γ-enolase and p-PI3K in ischemic brain. The cortical and subcortical sections show correspondingly decreased expression of γ-enolase and p-PI3K after 24 h of permanent ischemia. γ-enolase visualized by TRITC and p-PI3K was by FITC. Symbol # represent significant difference values p < 0.05, while symbols ∗∗ and ## represent p < 0.01 values for significant differences, symbol ∗∗∗ shows p < 0.001. Symbol ∗ shows significant difference relative to sham control while # shows significant difference relative to MCAO.