Skip to main content
. 2023 Jul 27;16(8):1065. doi: 10.3390/ph16081065

Figure 6.

Figure 6

Linagliptin inhibits hippocampal pro-apoptotic events in cadmium-intoxicated rats. Linagliptin downregulated Bax protein expression in hippocampal CA3 region (A,B), lowered caspase 3 activity (C), and increased the protein expression of the inactive form of the pro-apoptotic kinase GSK-3β (Ser9) (D) in the hippocampi of cadmium-intoxicated rats. (A) Representative immunohistochemistry images of Bax in hippocampal CA3 region (scale bar: 50 µm). (B) Bax protein quantitation (area %; 6 non-overlapping microscopic fields). Moreover, linagliptin upregulates Bcl-2 in hippocampal CA3 region in cadmium-intoxicated rats. (E) Representative immunohistochemistry images in hippocampal CA3 region (scale bar: 50 µm). (F) Bcl-2 protein quantitation (area %; 6 non-overlapping microscopic fields). N = 6 in each group (mean ± standard error of the mean). A p-value of less than 0.05 was significant. * p < 0.05, ** p < 0.01, *** p < 0.001, or **** p < 0.0001, compared to control; ## p < 0.01, ### p < 0.001, or #### p < 0.0001, compared to cadmium (Tukey’s test for multi-comparisons and one-way ANOVA). Bax, Bcl-2-associated x protein; Bcl-2, B-cell lymphoma-2 protein; Cd, cadmium chloride; GSK-3β, glycogen synthase kinase—3 beta; LIN, linagliptin.