Mechanism of the effect of Juan-Tong-Yin on endoplasmic reticulum stress-autophagy in endometriosis rats based on protein kinase R-like endoplasmic reticulum kinase/eukaryotic cell initiation factor 2α pathway

Qiyu Liu, Qi-Yu Liu, Jing Li, Feng-Qun Gu, Fengyun Meng, Feng-Yun Meng, Ying Liu, Wei-Hong Li, Weihong Li
Tissue & cell · 2025 · vol. 95 , pp. 102935 · doi:10.1016/j.tice.2025.102935 · PMID:40305948 · W4409799649
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This study investigated how Juan-Tong-Yin impacts endoplasmic reticulum stress-autophagy in endometriosis rats by examining the protein kinase R-like endoplasmic reticulum kinase/eukaryotic cell initiation factor 2α pathway.

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Abstract

OBJECTIVE: To explore the mechanism of Juan-Tong-Yin (JTY) on endoplasmic reticulum (ER) stress-autophagy in endometriosis (EM) rats through the protein kinase R-like endoplasmic reticulum kinase (PERK)/eukaryotic cell initiation factor 2α (eIF2α) autophagy pathway. METHODS: An EM rat model was established. A total of 70 Sprague-Dawley (SD) rats were randomly divided into the normal control group, model group, JTY high-, medium- and low-dose groups (25.4, 12.7, and 6.35 g/kg, respectively), progesterone group (0.26 mg/kg), and ER stress group (2-DG, 100 mg/kg). The seven groups were given the corresponding dose of the drug through gavage in the administration group and saline through gavage (1 mL/100 g) in the model and normal control groups. The drugs were administered continuously for 4 weeks. Ectopic lesion volume and pelvic adhesion score were measured. Hematoxylin-eosin (HE) staining was used to observe the pathological changes of ectopic endothelium in rats. Enzyme-linked immunosorbent assay (ELISA) was used to detect the levels of serum inflammatory marker C-reactive protein (CRP) and estradiol (E2) in each group; immunohistochemistry, real-time fluorescence quantitative polymerase chain reaction (Real-time PCR), and protein immunoblotting method (Western blotting) were used to detect the expressions of ectopic endothelial PERK, eIF2α, and microtubule-associated protein light chain 3B (LC3B) and mRNA. RESULTS: Compared with the model group, the JTY-treated rats exhibited significantly reduced ectopic lesion volume (P < 0.05), the pelvic adhesion score was decreased (P < 0.05), and the pathology of the ectopic endothelium showed varying degrees of atrophy, detachment, and gland reduction. In addition, serum inflammatory marker CRP and E2 levels were decreased significantly, and JTY promoted the expression of PERK, eIF2α, and microtubule-associated protein LC3B protein and mRNA (P < 0.05). CONCLUSION: JTY ameliorates EM by activating the PERK/eIF2a pathway, enhancing cell ER stress and autophagy, improving the inflammatory microenvironment, and ultimately mitigating EM in rats.

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Condition tags

endometriosis

MeSH descriptors

Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy Autophagy

Citation neighborhood

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References (30)

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