The protective effects of ritodrine against hypoxia/reoxygenation-induced injury in endometrial stromal cells

Jing Zhu, Zhu J, Haiyun Liu, Liu H, Lijing Mao
Human & experimental toxicology · 2022 · vol. 41 , pp. 9603271221120650 · doi:10.1177/09603271221120650 · PMID:36000350 · W4292997387
article OA: diamond CC0 ⤵ 2 in-corpus citations
📄 Open PDF View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Ritodrine ameliorated hypoxia/reoxygenation-induced injury in human endometrial stromal cells by inhibiting the ER-α/NF-κB pathway and reducing oxidative stress and inflammation.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

Abstract

Endometriosis (EMS) is often observed in women of childbearing age and significantly impacts patients' quality of life. Ritodrine is a β2 receptor agonist applied for relaxing the uterine smooth muscle. Its inhibitory effects on inflammation have recently been noted. The present study explored the protective impact of Ritodrine on hypoxia/reoxygenation (H/R)- induced injury in endometrial stromal cells (ESCs). Human ESCs (HESCs) were treated with Ritodrine (0.1, 0.5 μM) for 24 h, followed by exposure to H/R for 6 h. Ritodrine ameliorated H/R-induced higher reactive oxygen species (ROS), declined glutathione (GSH) concentration and increased production of tumor necrosis factor-α (TNF-α), interleukin- 6 (IL-6), and monocyte chemotactic protein 1 (MCP-1) in HESCs. Furthermore, Ritodrine ameliorated the H/R-induced higher nuclear level of nuclear factor κ-B (NF-κB) p65 expression and increased luciferase activity of the NF-κB promoter. In addition, we show that Ritodrine mitigated H/R-induced higher estrogen receptor α (ER-α) expression in HESCs. Interestingly, overexpressing ER-α abolished the regulatory effects of Ritodrine on oxidative stress and the NF-κB pathway-mediated inflammation. Collectively, our data reveal that Ritodrine alleviated H/R-induced injury in ESCs by inhibiting the ER-α/NF-κB pathway.

My notes (saved in your browser only)

Condition tags

endometriosis

MeSH descriptors

NF-kappa B NF-kappa B NF-kappa B NF-kappa B NF-kappa B NF-kappa B NF-kappa B NF-kappa B NF-kappa B NF-kappa B NF-kappa B NF-kappa B NF-kappa B NF-kappa B NF-kappa B NF-kappa B NF-kappa B NF-kappa B NF-kappa B NF-kappa B

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (41)

Cited by (2)

Source provenance

europepmc
last seen: 2026-07-27T06:15:28.040536+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-07-27T06:15:20.614192+00:00
License: CC0 · commercial use OK