Protective Effect and Mechanism of Total Saponins of Codonopsis Radix on Cognitive Dysfunction in Aging Mice
10.13422/j.cnki.syfjx.20241203
- VernacularTitle:党参总皂苷对衰老小鼠认知功能障碍保护作用及机制
- Author:
Chongyang ZHANG
1
;
Miao YU
1
;
Rongchang CHEN
2
;
Bin ZHANG
2
;
Xiaobo SUN
2
;
Zunpeng SHU
1
Author Information
1. School of Traditional Chinese Medicine，Guangdong Pharmaceutical University，Guangzhou 510006，China
2. Pharmacology and Toxicology Center，Institute of Medicinal Plant Development， Chinese Academy of Medical Sciences，Beijing 100193，China
- Publication Type:Journal Article
- Keywords:
total saponins of Codonopsis Radix;
inflammation;
aging;
cognitive function;
oxidative stress
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2024;30(20):70-76
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the ameliorative effect and mechanism of total saponins of Codonopsis Radix （TSC） on learning and memory impairment induced by D-galactose in aging mice. MethodTwenty-four male C57BL/6J mice were randomly assigned into four groups （n=6）： normal group， model group （200 mg·kg-1 D-galactose）， TSC group （200 mg·kg-1）， and donepezil group （3 mg·kg-1）. After one week of pre-treatment， the mice in the model， TSC， and donepezil groups were administrated with corresponding agents for 8 weeks. In the ninth week， the Morris water maze test was performed to assess the learning and memory abilities. Histopathological changes in the brain were evaluated by hematoxylin-eosin （HE） and Nissl staining. Immunohistochemistry was used to detect the expression of nuclear factor kappa-B （NF-κB）， tumor necrosis factor-α （TNF-α）， and brain-derived neurotrophic factor （BDNF） in the brain tissue. The serum levels of glutathione peroxidase （GSH-Px）， catalase （CAT）， superoxide dismutase （SOD）， malondialdehyde （MDA）， TNF-α， interleukin-1β （IL-1β）， and interleukin-18 （IL-18） were measured by enzyme-linked immunosorbent assay， on the basis of which the effects of TSC on neuroinflammation and memory impairment in D-galactose-induced aging mice were assessed. ResultCompared with the normal group， the model group exhibited decreased cognitive function， decreased activities of CAT， SOD， and GSH-Px in the serum （P<0.01）， and upregulated levels of MDA， TNF-α， IL-1β， and IL-18 （P<0.01）. In addition， partial neuronal damage and degeneration were observed in the hippocampus and cortex of the model group， accompanied by downregulated BDNF expression （P<0.05） and upregulated NF-κB and TNF-α expression （P<0.05）. Compared with the model group， TSC alleviated D-galactose-induced cognitive dysfunction， enhanced the activities of CAT， SOD， and GSH-Px （P<0.01）， lowered MDA， TNF-α， IL-1β， and IL-18 levels （P<0.01）， and ameliorated the pathological changes in the hippocampus and cerebral cortex. Additionally， TSC upregulated BDNF expression （P<0.05， P<0.01） and downregulated NF-κB and TNF-α expression （P<0.05， P<0.01） in the hippocampus and cerebral cortex. ConclusionTSC exerts a protective effect on cognitive dysfunction induced by D-galactose in aging mice by inhibiting oxidative stress and inflammation.
