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

Figure 10  Troxerutin improves mitochondrial energy metabolism abnormality and cell apoptosis induced by high-concentration glucose in hippocampal neuronal cells. A: Relative of adenosine triphosphate level; B: The normalized mRNA expression of caspase-3, B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax), and Bcl-2; C: The red fluorescence increased in the diabetes + troxerutin group, indicating an increase in mitochondrial membrane potential and a decrease in apoptotic cells; D: The relative protein expression of caspase-3, Bcl-2-associated X protein, and Bcl-2. Consistent with the animal results, the aforementioned effect of troxerutin was attenuated after overexpressing transient receptor potential melastatin 7. ^aP < 0.05, compared with normal control group; ^bP < 0.05, compared with high-concentration glucose group; ^cP < 0.05, compared with high-concentration glucose + troxerutin group. Data presented as mean ± SEM. TRPM7: Transient receptor potential melastatin 7; ATP: Adenosine triphosphate; NC: Normal control; HG: Hypertonic group; T: Troxerutin; Bax: B-cell lymphoma 2-associated X protein; Bcl-2: B-cell lymphoma 2.