Abstract
Background and Objective: Diabetes is fundamentally connected with the inability of cognition. Chlorogenic acid (CGA) has multiple biologic functions and is diffusely utilized in diabetic complications. The current study aimed to explore the improvement effect of CGA on cognitive deficits in diabetic rats. Materials and Methods: The model of the diabetic rat was constituted by STZ (50 mg kg–1). The experiment rats were treated with CGA (30 mg kg–1/day) by gastric perfusion for 8 weeks. After the last treatment, Morris water maze was examined to estimate cognitive function. In hippocampus tissue, the spectrophotometer was performed to evaluate SOD, CAT, GSH and MDA levels. The qRT-PCR and ELISA were utilized to analyze TNF-α and IL-1β contents. Western blot was used to detect the protein expressions of BDNF, GFAP Nrf-2 and HO-1. Results: Current data demonstrated that CGA reduced escape latency and increased times of crossing platform in Morris water maze test to improve diabetic-induced learning and memory impairments. CGA inhibited AChE and GFAP expressions, while augmented ChAT, BDNF, Nrf-2 and HO-1 expressions in the hippocampus. Moreover, CGA promoted SOD, CAT and GSH levels and suppressed MDA concentration to mitigate oxidative stress. Meanwhile, CGA inhibited TNF-a and IL-1β contents to relieve inflammatory response. Lastly, CGA restrained Bax/Bcl-2 ratio to alleviate apoptosis. Conclusion: CGA protected against diabetic-induced learning and memory impairments via improvement of oxidative stress, inflammation and apoptosis and could be used as a novel therapeutic in the prevention and treatment of DACD.
