Figure 3.

Western blot assay of GSK3β at different phosphorylation sites in response to STZ, geniposide and WT treatment was shown in A. Total GSK3β protein was shown in the histograms of brain cortex (B). Quantitative analysis shows that no significant difference on the total expression of GSK3β among the five treatment groups (B). Phospho‐GSK3β (inactive) and (active) was presented as the ratio over loading control (β‐Actin). GSK3β activity did not differ between rats treated with aCSF and Geniposide alone (C,D). STZ alone significantly elevated GSK3β activity compared with controls as reflected with increased pGSK3β^Y216 (C, *, compared with control, P < 0.01) and decreased pGSK3β^S9 (D, *, compared with control, P < 0.01). STZ + Geniposide prevented STZ‐induced increase in GSK3β activity, reflected as lower ratio of pGSK3β^Y216 (C, #, compared to STZ‐alone group, P < 0.01) and higher ratio of pGSK3β^S9 (D, # compared to STZ‐alone group, P < 0.01). PI3K inhibitor WT blocked the protective effect of geniposide, reflected as higher ratio of pGSK3β^Y216 (C, + compared to STZ + Geni, P < 0.01) and lower ratio of pGSK3β^S9 (D, + compared to STZ + Geni, P < 0.01).