Naringin ameliorates cognitive deficits via oxidative stress, proinflammatory factors and the PPARγ signaling pathway in a type 2 diabetic rat model

Abstract

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 curcumin 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 γ (PPARγ) were quantified in the DM rats using a commercially‑available kit and western blot assay, respectively. In addition, a GW9662 PPARγ inhibitor (0.3 mg/kg) was administered to the DM rats to determine whether PPARγ 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 PPARγ, and administration of the PPARγ inhibitor decreased the protein expression of PPARγ, 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 PPARγ signaling pathway in the type 2 diabetic rat model. Furthermore, oxidative stress, proinflammatory factors and PPARγ signaling may be involved in mediating these effects.

Naringin provides neuroprotection in CCL2-induced cognition impairment by attenuating neuronal apoptosis in the hippocampus

“…These results revealed the antioxidative stress effects of naringin. In fact, a few reports have revealed that naringin could ameliorate cognitive deficits by enhancing antioxidative stress [29,31], as demonstrated by our current results. In addition, our previous studies have observed that CCL2 can enhance NMDA receptor-mediated EPSC and mediate Ca 2+ influx [12,32].…”

“…9 Naringin improves CCL2-induced cognition impairment mechanism illustration. Naringin treatment inhibited the oxidation, inflammation, reducing excitotoxicity and ultimately alleviating neurons apotosis and damage in rats with learning and memory impairment [16,29]. Therefore, elevated SOD and GSH-Px activities could directly reflect a powerful antioxidative ability.…”

Naringin, a natural dietary compound, prevents intestinal tumorigenesis in Apc Min/+ mouse model

“…Naringin ameliorates sodium arsenite-induced renal and hepatic toxicity in rats by modulating the activities of KIM-1, caspase-3, TGF-β and TNF-α (Adil et al 2015). Naringin ameliorates cognitive deficits via oxidative stress, proinflammatory factors and the PPARγ signaling pathway in a type 2 diabetic rat model (Qi et al 2015). Naringin protects neural cells on 3-nitropropionic acid-induced mitochondrial dysfunction through modulation of Nrf2 signaling pathway (Kulasekaran and Ganapasam 2015).…”

Naringin Reveals Ameliorative Property Over Elevated Oxidative Stress Levels in Animal Models

“…Oral administration of NG (10, 20, and 40 mg/kg) to isoproterenol exposed Wistar rats showed a considerable decrease in the levels of lipid peroxidation products and improved the antioxidant status [47]. NG is known for its anti-inflammatory [46,[48][49][50] and antioxidative nature [43,45,51,52]. Arsenic-induced hepatic and renal toxicity are reported to be reduced by anti-inflammatory and antioxidative nature of NG [53].…”

“…An experimental diabetes mellitus rat model was induced by streptozoticin (50 mg/kg) and NG treatment (100 and 200 mg/kg) for 16 weeks was given. A Morris water maze test was used to analyze the effects of NG on the cognitive deficit, and the results demonstrated that NG ameliorated cognitive deficits through OxiS, pro-inflammatory factors, and the peroxisome proliferatoractivated receptor gamma signaling pathway in the Type 2 diabetic rat model [52].…”