Ursolic acid mitigates cognitive dysfunction through amelioration of oxidative stress, inflammation and apoptosis in diabetic rats


 Purpose: To determine the effect of ursolic acid (UA) on diabetes-induced cognitive defect, as well its mechanism action in streptozotocin (STZ)-induced diabetic rats.
 Methods: A rat model diabetes was established by administration STZ. The rats received UA via gastric perfusion for 56 successive days. Learning and memory functions were assessed using Morris water maze. Superoxide dismutase (SOD) activity malondialdehyde (MDA) levels hippocampus tissues determined spectrophotometrically. Tumor necrosis factor-a (TNF-a), interleukin-1β (IL-1β) interleukin-6 (IL-6) assayed quantitative real-time polymerase chain reaction (qRT- PCR) enzyme-linked immunosorbent assay (ELISA). protein expression nuclear factor erythroid-2-related factor-2 (Nrf-2), heme oxygenase-1 (HO-1), Bcl-2 Bax evaluated western blotting.
 Results: impairment STZ-induced mitigated (p < 0.05). In tissue, reduced oxidative stress enhancing SOD reducing MDA levels. Furthermore, inflammatory response downregulating TNF-α, IL-1β IL-6 Concomitantly, lower concentrations Nrf-2 HO-1 elevated UA. suppressed Bax/Bcl-2 ratio to ameliorate apoptosis 0.05).
 Conclusion: reduces hippocampal stress, inflammation apoptosis. Thus, it might be a potential drug candidate delaying diabetes-associated decline (DACD).