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Emodin Promoted Intestinal Secretion of GLP-1 and Limited Cognitive Deficits in Young Bilateral Ovariectomized Rats.

Xin-Yuan Liu1, Chao-Yuan Ye1, Yuan-Cheng Liu1,2

  • 1Key Laboratory of Neurological Disease of Hubei Province and National Education Ministry, Department of Pathology and Pathophysiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

International Journal of Molecular Sciences
|May 4, 2026
PubMed
Summary

Emodin (EMO) treatment improves cognitive and emotional deficits in ovariectomized rats by increasing glucagon-like peptide-1 (GLP-1) levels via an estrogen receptor beta-dependent pathway, offering a potential alternative to estrogen therapy.

Keywords:
GLP-1PCSK1emodinestrogen receptor βproGCG

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Area of Science:

  • Neuroscience
  • Endocrinology
  • Pharmacology

Background:

  • Estrogen deficiency after menopause contributes to brain dysfunction in women.
  • There is a need for treatments that address estrogen deficiency-related brain issues without estrogen supplement side effects.

Purpose of the Study:

  • To investigate the potential of emodin (EMO) in ameliorating brain dysfunction caused by estrogen deficiency in a rat model.
  • To explore the underlying mechanisms involving glucagon-like peptide-1 (GLP-1) and estrogen receptors (ER).

Main Methods:

  • Ovariectomy (OVX) was performed on rats, followed by treatment with EMO or 17 β-estradiol (EST).
  • Cognitive and emotional behaviors were assessed, alongside measurements of blood GLP-1 and estrogen levels.
  • mRNA levels of ERα, ERβ, GLP-1 receptor (GLP-1R), PCSK1, and proGCG in intestinal and brain tissues were analyzed.
  • Intestinal contractility and the effects of an ERβ antagonist (PHTPP) were examined.

Main Results:

  • EMO and EST treatments significantly improved cognitive deficits and depressive behaviors in OVX rats.
  • EMO increased blood GLP-1 levels through an ERβ-dependent mechanism in the intestine and elevated brain GLP-1R levels.
  • EMO demonstrated neuroprotective effects in the hippocampus and prefrontal cortex, reducing neuronal loss and synaptic abnormalities.

Conclusions:

  • Emodin effectively ameliorates estrogen deficiency-induced brain dysfunction in OVX rats.
  • The mechanism involves up-regulation of the GLP-1 pathway via intestinal ERβ.
  • EMO represents a promising therapeutic candidate for menopausal brain disorders.