Troxerutin improves diabetic cognitive dysfunction by inhibiting mitochondrial fission mediated by transient receptor potential melastatin 7/calcineurin/dynamin-related protein 1ser637

Figure 9 Troxerutin improved mitochondrial fission and cell apoptosis in the hippocampal tissue of diabetic cognitive dysfunction mice. A: Transmission electron microscopy images show a decrease in mitochondrial fission in the hippocampal tissue of db-T group compared to db group; B: The length and width of mitochondria were measured (n = 20); C: Hematoxylin and eosin staining shows that hippocampal pyramidal cells injury was improved in db-T group compared to db group (400 ×); D: Relative of adenosine triphosphate level; E: The normalized mRNA expression of caspase-3, B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax), and Bcl-2; F: The relative protein expression of The relative protein expression of caspase-3, Bcl-2-associated X protein, and Bcl-2. Bradykinin is a transient receptor potential melastatin 7 agonist, and its addition diminished the neuroprotective effect of troxerutin. ^aP < 0.05, compared with dm group; ^bP < 0.05, compared with diabetes group; ^cP < 0.05, compared with diabetes + troxerutin group. Data presented as mean ± SEM. dm: Control group; dm-T: Control + troxerutin group; db: Diabetes group; db-T: Diabetes + troxerutin group; db-T-B: Diabetes + troxerutin + bradykinin group; Bax: B-cell lymphoma 2-associated X protein; Bcl-2: B-cell lymphoma 2.