Research on the improvement of cognitive impairment,endoplasmic reticulum stress and neuroinflammation in Alzheimer's disease by emodin
10.3969/j.issn.1674-8115.2025.06.007
- VernacularTitle:大黄素改善阿尔茨海默病认知障碍、内质网应激和神经炎症的研究
- Author:
Le YANG
1
;
Yi ZHOU
;
Keyun WANG
;
Yali LAI
Author Information
1. 成都医学院第二附属医院,核工业四一六医院神经内科,成都 610041
- Publication Type:Journal Article
- Keywords:
Alzheimer's disease(AD);
emodin;
neuroinflammation;
endoplasmic reticulum stress
- From:
Journal of Shanghai Jiaotong University(Medical Science)
2025;45(6):727-734
- CountryChina
- Language:Chinese
-
Abstract:
Objective·To explore the effects and potential mechanisms of emodin on Alzheimer's disease(AD).Methods·Wild-type C57BL/6J mice and 3×Tg-AD mice were divided into 6 groups:Control group(C57BL/6J mice),AD group(3×Tg-AD mice),Emodin 25 mg/kg group(3×Tg-AD mice+Emodin 25 mg/kg),Emodin 50 mg/kg group(3×Tg-AD mice+Emodin 50 mg/kg),Emodin 100 mg/kg group(3×Tg-AD mice+Emodin 100 mg/kg)and Donepezil group(3×Tg-AD mice+Donepezil 3 mg/kg).The Morris water maze test was used to evaluate the learning and memory abilities of mice.The expression of glial fibrillary acidic protein(GFAP),glucose-regulated protein 78kDa(GRP78),and inositol-requiring enzyme 1α(IRE1α)was detected by immunohistochemistry.The levels of tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),and IL-6 in brain tissue were measured by enzyme-linked immunosorbent assay(ELISA).Western blotting was used to detect the expression of NF-κB p65,p-NF-κB p65,p38,and p-p38 proteins.Results·Compared with the control group,mice in the AD group showed impaired cognition,increased GFAP expression,elevated levels of TNF-α,IL-1β and IL-6,and increased expression of GRP78 and IRE1α,along with enhanced phosphorylation of NF-κB p65 and p38.Compared with the AD group,emodin improved cognitive impairment of AD mice,inhibited astrocyte overactivation and neuroinflammation,and decreased the expression of GRP78,IRE1α,phosphorylated NF-κB p65,and phosphorylated p38 in brain tissue.Conclusion·Emodin can effectively improve cognitive impairment in AD mice,which may be related to the inhibition of endoplasmic reticulum stress-mediated neuroinflammation in astrocytes.
