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. Author manuscript; available in PMC: 2016 Apr 30.
Published in final edited form as: Cell Physiol Biochem. 2015 Apr 30;36(1):208–220. doi: 10.1159/000374065

Fig. 2.

Fig. 2

NSC23766 administration protects diabetes-induced p38 MAP kinase in mouse retina. Panel A. Retinal proteins from normal, diabetic and diabetic mice treated with NSC23766, a specific inhibitor of Tiam1-Rac1 signaling pathway [6], were separated by SDS-PAGE and the relative abundance of phosphorylated (p-p38) and total (t-p38) p38 MAP kinase was determined by Western blotting. Fold increase in the ratios of p-p38 to t-p38 are shown here. Panel B. Immunostaining of p38 MAP kinase was performed in the 10μm thick retinal cryosections using anti-p38 antibody (green), and DAPI (blue) was used to stain the nuclei. The sections were imaged at 20X magnification using Olympus BX50 fluorescent microscope. The images presented here are representative of 3 or more mice in each group. Panel C represents the fluorescence intensity, quantified by using ImageJ software. Norm=Normal, Diab=Diabetes and Diab+NSC= diabetic mice receiving NSC23766. ONL and GCL= Outer nuclear layer and ganglion cell layer respectively. The data are mean ± SEM from four animals in each group. *P < 0.001 vs. normal and **P < 0.001 vs. diabetic.