Naringin ameliorates memory deficits and exerts neuroprotective effects in a mouse model of Alzheimer's disease by regulating multiple metabolic pathways

Abstract

The aim of the present study was to investigate the neuroprotective effects of naringin on the memory impairment of hydrocortisone mice, and to elucidate the potential underlying molecular mechanisms. In the present study, a hydrocortisone model was constructed. Novel object recognition, Morris water maze and step-down tests were performed in order to assess the learning and memory abilities of mice. Hematoxylin and eosin staining was used to observe pathological changes in the hippocampus and hypothalamus. Transmission electron microscopy was used to observe the ultrastructural changes in the hippocampus. Immunohistochemistry was used to detect the expression of ERα and ERβ. Western blotting was performed to detect the expression of each protein in the relevant system. It was found that naringin can significantly improve cognitive, learning and memory dysfunction in mice with hydrocortisone memory impairment. In addition, naringin can exert neuroprotective effects through a variety of mechanisms, including amyloid β metabolism, Tau protein hyperphosphorylation, acetylcholinergic system, glutamate receptor system, oxidative stress and cell apoptosis. Naringin can also affect the expression of phosphorylated-P38/P38, indicating that the neuroprotective effect of naringin may also involve the MAPK/P38 pathway. The results of the present study concluded that naringin can effectively improve the cognitive abilities of mice with memory impairment and exert neuroprotective effects. Thus, naringin may be a promising target drug candidate for the treatment of Alzheimer's disease.

Neuroprotective effect of naringin against cerebellar changes in Alzheimer’s disease through modulation of autophagy, oxidative stress and tau expression: An experimental study

“…After 2 weeks of acclimatization, the rats were divided into four groups (n = 6/group): (i) Control (C) received saline per oral (p.o. ), (ii) Naringin(N)-received naringin (100 mg/kg/d) p.o (Meng et al, 2021), (iii) AlCl 3 -recived AlCl 3 (100 mg/kg/d) p.o (Lakshmi et al, 2015), and (iv) AlCl 3 + Naringin (AlCl 3 + N) received both AlCl 3 and naringin p.o for 21 days. At the end of experiment, body weight was measured and Rotarod and Morris water maze tests were conducted to assess motor and learning abilities, respectively.…”

Naringin Improves Osteoblast Mineralization and Bone Healing and Strength through Regulating Estrogen Receptor Alpha-Dependent Alkaline Phosphatase Gene Expression

“…A docking study revealed that naringin can interact with certain amino acids of ERα, similar to the binding sites of estrogen . In an animal model of Alzheimer’s disease, naringin exerted neuroprotective effects and also improved the cognitive ability of mice via upregulating ERα and ERβ expression . The ERα signaling pathway contributes to osteoblast maturation through upregulating ATP production-linked gene expression .…”

“…51 In an animal model of Alzheimer's disease, naringin exerted neuroprotective effects and also improved the cognitive ability of mice via upregulating ERα and ERβ expression. 57 The ERα signaling pathway contributes to osteoblast maturation through upregulating ATP production-linked gene expression. 26 Furthermore, our preceding study exhibited that suppressing the ERα signaling could slow down energy metabolism, osteoblast differentiation, and angiogenesis and delay bone regeneration.…”

Effect of Noni on Memory Impairment Induced by Hydrocortisone in Mice

“…Forty-eight male Kunming mice were divided into 6 groups using a random number table, with 8 in each group: the control group, the model group (double distilled water 10 mL/kg/day), the ginseng group (1 g/kg/day), the high-dose noni group (1.33 g/kg/day, H-noni), the middle-dose noni group (0.67 g/kg/day, M-noni), and the low-dose noni group (0.33 g/kg/day, L-noni). In the morning, forty rats were given hydrocortisone (25 mg/kg/day) by gastric gavage for 14 consecutive days to establish the memory impairment model [ 16 ], except for those in the control group. On the same day, the corresponding drugs were administered by gastric gavage in the afternoon.…”