ArticleImmunity, inflammation and disease2023
Oxycodone alleviates mifepristone-stimulated human endometrial stromal cell injury by activating the Keap1/Nrf2/HO-1 signaling pathway.
Article in Immunity, inflammation and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- [Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2026Article
- Bushen Zhuyun Decoction Enhances Endometrial Receptivity via the IL-6/STAT3 Signaling Pathway in Rats.Combinatorial chemistry & high throughput screening · 2025Article
- An Overview of Bioactive Compounds' Role in Modulating the Nrf2/Keap1/NF-κB Pathway to Alleviate Lipopolysaccharide-Induced Endometritis.International journal of molecular sciences · 2024Review
- Oxycodone alleviates mifepristone-stimulated human endometrial stromal cell injury by activating the Keap1/Nrf2/HO-1 signaling pathway.Immunity, inflammation and disease · 2023Article
- Exploring the protective effects of ischelium on rat brain ischemia-reperfusion injury.Science progressArticle
- Oxycodone attenuates endotoxin-induced acute lung injury by regulating mitophagy via the HO-1 pathway.Clinics (Sao Paulo, Brazil)Article
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3 authors.
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Abstract
backgroundEndometrial injury is a common disease in women caused by intrauterine inflammation, infections, and endocrine disorders. Human endometrial stromal cells (hEndoSCs) can maintain endometrial homeostasis and play an important role in repairing endometrial injury. Mifepristone, a steroidal anti-progesterone drug, is widely used in the field of reproductive medicine worldwide. Mifepristone-induced hEndoSC injury has been used to study endometrial injury in vitro. At present, the pathogenesis and potential regulatory mechanisms of oxycodone in endometrial injury remain unknown.
aimsWe aimed to evaluate the functions of oxycodone in mifepristone-stimulated hEndoSC injury and analyze its potential molecular mechanism. MATERIALS &
methodshEndoSC viability, cytotoxicity, and apoptosis were analyzed using the methyl thiazolyl tetrazolium assay, the lactate dehydrogenase assay, and flow cytometry, respectively. Furthermore, the levels of cleaved-Caspase3, Keap1, Nrf2, HO-1, and NQO1 were assessed using reverse transcription quantitative polymerase chain reaction and western blot analysis, and the release of inflammatory cytokines was determined using the enzyme-linked immunosorbent assay.
resultsWe observed that oxycodone had no adverse effects on hEndoSCs; rather, it protected hEndoSCs against mifepristone-induced endometrial damage, as confirmed by the enhanced cell viability, reduced number of apoptotic cells, decreased Caspase3 activity and inflammatory cytokine secretion, and increased Keap1/Nrf2/HO-1 pathway-related protein expression. In addition, we found that the protective effects of oxycodone on mifepristone-induced hEndoSC injury were inhibited by ML385 (a Keap1/Nrf2/HO-1 inhibitor).
conclusionIn summary, we confirmed that oxycodone alleviates mifepristone-induced hEndoSC injury by activating the Keap1/Nrf2/HO-1 signaling pathway.
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