Abstract
Background and Objective: Diabetes is closely connected with abnormity of cognitive performance. Asiatic acid (AA) has various bioactivities and possesses preventive, protective and therapeutic functions in diabetic progression. However, no research has implied the prevention and treatment of AA on cognitive performance in diabetes. Materials and Methods: In this research, the diabetic rat model was established by STZ to appraise potentially therapeutic options of AA (30 mg/kg/day for 45 days) on diabetes-associated cognitive decline (DACD). After the last treatment, rats were euthanized to collect the hippocampus for mechanism research. Results: Current research demonstrated AA decreased escape latency and enhanced times of crossing platform to protect against diabetic-evoked cognitive dysfunctions. In the hippocampus, AA remarkably restricted AChE and GFAP expressions, while promoting ChAT, BDNF, Nrf-2 and HO-1 expressions. Moreover, AA remarkably augmented SOD, CAT and GSH contents and restrained MDA concentration to alleviate oxidative stress. Additionally, AA remarkably inhibited TNF-α and IL-1β productions to mitigate inflammatory response. Lastly, AA remarkably reduced Bax expression and increased Bcl-2 expression to relieve apoptosis. Conclusion: AA protected the hippocampus from diabetic-evoked cognitive dysfunctions through its bioactivities of anti-oxidation, anti-inflammation and anti-apoptosis and could be a powerful remedy approach in the ameliorations of DACD.