Naringin Ameliorates Cognitive Deficits Via Oxidative Stress, Proinflammatory Factors And The Ppar Gamma Signaling Pathway In A Type 2 Diabetic Rat Model

Naringenin is a flavonoid polyphenolic compound, which facilitates the removal of free radicals, oxidative stress and inflammation. The present study aimed to obtain. a better understanding of the effects of Naringin on the regulation of diabetes-associated cognitive decline, and its underlying mechanisms. An experimental diabetes mellitus (DM) rat model was induced by streptozoticin (50 mg/kg). Following treatment with naringin (100 and 200 mg/kg) for 16 weeks, the body weight and blood glucose levels of the DM rats were measured. A morris water maze test was used to analyze the effects of naringin on the cognitive deficit of the DM rats. The levels of oxidative stress, proinflammatory factors, caspase-3 and caspase-9, and the protein expression of peroxisome proliferator-activated receptor gamma (PPAR gamma) were quantified in the DM rats using a commercially-available kit and western blot assay, respectively. In addition, a GW9662 PPAR gamma inhibitor (0.3 mg/kg) was administered to the DM rats to determine whether PPAR gamma affected the effects of naringin on the cognitive deficit of the DM rats. The results demonstrated that naringin increased the body weight, blood glucose levels, and cognitive deficits of the DM rats. The levels of oxidative stress and proinflammatory factors in the naringin-treated rats were significantly lower, compared with those of the DM rats. In addition, naringin activated the protein expression of PPAR gamma, and administration of the PPAR gamma inhibitor decreased the protein expression of PPAR gamma, and attenuated the effects of naringin on cognitive deficit. The results also demonstrated that naringin decreased the expression levels of caspase-3 and caspase-9 in the DM rats. These results suggested that naringin ameliorated cognitive deficits via oxidative stress, proinflammatory factors and the PPAR gamma signaling pathway in the type 2 diabetic rat model. Furthermore, oxidative stress, proinflammatory factors and PPAR gamma signaling may be involved in mediating these effects.