Journal of Shanghai Jiao Tong University (Medical Science) >

2025 , Vol. 45 >Issue 6: 727 - 734

DOI: https://doi.org/10.3969/j.issn.1674-8115.2025.06.007

Basic research

Research on the improvement of cognitive impairment, endoplasmic reticulum stress and neuroinflammation in Alzheimer's disease by emodin

  • YANG Le ,
  • ZHOU Yi ,
  • WANG Keyun ,
  • LAI Yali
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  • 1.Department of Neurology, The Second Affiliated Hospital of Chengdu Medical College, 416 Nuclear Industry Hospital, Chengdu 610041, China
    2.Department of Neurology, Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, Chengdu 610072, China
First author contact:YANG Le and ZHOU Yi participated in the experimental design. YANG Le, ZHOU Yi and WANG Keyun participated in experimental operations, data collection, and data analysis. YANG Le, ZHOU Yi, WANG Keyun and LAI Yali participated in the writing and editing of the paper. All authors have read and agreed to submit the final manuscript.
LAI Yali, E-mail: 838856089@qq.com.

Received date: 2024-11-18

  Accepted date: 2025-02-18

  Online published: 2025-06-28

Supported by

2020 Sichuan Province Health Research Project(20ZD009)

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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.

Key words： Alzheimer's disease (AD); emodin; neuroinflammation; endoplasmic reticulum stress

Cite this article

YANG Le , ZHOU Yi , WANG Keyun , LAI Yali . Research on the improvement of cognitive impairment, endoplasmic reticulum stress and neuroinflammation in Alzheimer's disease by emodin[J]. Journal of Shanghai Jiao Tong University (Medical Science), 2025 , 45(6) : 727 -734 . DOI: 10.3969/j.issn.1674-8115.2025.06.007

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