Effects of Naringin on neuronal apoptosis in mice with memory consolidation disorder
10.3760/cma.j.cn115398-20200807-00056
- VernacularTitle:柚皮苷对记忆巩固障碍模型小鼠神经细胞凋亡的影响
- Author:
Xia LEI
1
;
Deping ZHAO
;
Yumo WANG
;
Ting SUN
;
Ning ZHANG
;
Hongbin XIAO
Author Information
1. 黑龙江中医药大学佳木斯学院 150040
- Keywords:
Naringin;
Memory consolidation disability;
Glutamic acid;
Acetyl choline;
Oxidative stress;
Apoptosis;
Mice
- From:
International Journal of Traditional Chinese Medicine
2021;43(10):986-992
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To observe the effect of Naringin on neuronal apoptosis in mice with memory consolidation disorderinduced by sodium nitrite.Methods:Fifty mice were randomly divided into blank group, model group, standardized protocol group, high-dose Naringin group and low-dose Naringin group, with 10 mice in each group. The standardized protocol group was given Donepezil 1 mg/kg, the Naringin high and low dose groups were gavaged with Naringin solution 100 and 50 mg/(kg·d), blank group and model group were gavaged with equal volume of distilled water once a day for 21 days. The model was established on the 22nd day. The blank group was intraperitoneally injected with normal saline, and the other groups were intraperitoneally injected with 100 mg/(kg·d) sodium nitrite solution for 7 days. The cognitive ability of mice in each group was evaluated by platform jumping test, and the hippocampal synaptic structure was observed by electron microscope. The contents of acetylcholine (ACh), SOD, MDA and NO in hippocampus and the activity of choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) was detected by ELISA. The expression of N-methyl-D-aspartate receptor (NMDAR), glutamine receptor 2 (GluR), calcium/calmodulin dependent protease Ⅱ (CaMK Ⅱ), Caspase-3, Bcl-2 and Bad proteins in hippocampus of model mice were detected by Western blot.Results:The number and morphology of hippocampal neurons were normal, nucleus, mitochondria, rough endoplasmic reticulum and synaptic membrane of hippocampal neurons in high-dose Naringin group were clear. Compared with the model group, the latency of mice in the high-dose Naringin group was prolonged and the number of errors was reduced ( P<0.01). The levels of MDA and NO in hippocampus of mice in the high-dose Naringin group significantly decreased ( P<0.01), and the activity of SOD significantly increased ( P<0.01). The content of ACh (23.682 ± 2.835 μg/mg prot vs. 14.939 ± 2.901 μg/mg prot), ChAT (163.302 ± 21.278 U/g vs. 89.612 ± 11.497 U/g) increased, AChE (0.367 ± 0.015 U/mg prot vs. 0.471 ± 0.014 U/mg prot) activity decreased ( P<0.01); The expression of Bad (0.441 ± 0.010 vs. 0.633 ± 0.010), Caspase-3 (0.425 ± 0.036 vs. 0.537 ± 0.024) significantly decreased, and the expression of Bcl-2 (0.890 ± 0.014 vs. 0.727 ± 0.009) significantly increased ( P<0.01); The expression of CAMKⅡ (1.043 ± 0.037 vs. 1.475 ± 0.043) significantly decreased ( P<0.01), and the expression of NMDAR1 (0.407 ± 0.037 vs. 0.345 ± 0.012), GluR2 (1.125 ± 0.033 vs. 0.664 ± 0.023) significantly increased ( P<0.01). Conclusion:Naringin could play the role of protecing the neuron and improving the cognition of mice with memory consolidation disorder by regulating the balance of ACh and glutamate system and reducing neuronal apoptosis and antioxidant stress.
