Constitutive and tumor necrosis factor-α-induced activation of nuclear factor-κB in adenomyosis and its inhibition by andrographolide

Lab / animal OA: closed CC0 ⤵ 49 in-corpus citations
View on OpenAlex View on PubMed View at publisher
⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-06-10 ⓘ

This study investigated the activation of nuclear factor-κB in adenomyosis and found it could be inhibited by andrographolide.

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

Abstract

OBJECTIVE: To investigate the action of nuclear factor (NF)-κB in adenomyosis and evaluate the potential therapeutic effect of andrographolide on tumor necrosis factor (TNF)-α-induced expression of NF-κB-mediated genes cyclooxygease-2 (COX-2), vascular endothelial growth factor (VEGF), and tissue factor (TF) in adenomyotic stromal cells. DESIGN: Laboratory study using human tissues. SETTING: Academic hospital. PATIENT(S): Twenty-nine patients (cases) with histologically confirmed adenomyosis and 14 (controls) without adenomyosis or endometriosis. INTERVENTION(S): Endometrial stromal cells derived from tissue samples harvested from both cases and controls were subjected to electrophoretic mobility shift assay, and gene and protein expression analyses. MAIN OUTCOME MEASURE(S): The NF-κB DNA-binding activity and protein levels of NF-κB subunits p50 and p65 and the messenger RNA (mRNA) and protein levels of NF-κB-mediated genes COX-2, VEGF, and TF in cases and controls, and their changes after stimulation with TNF-α and treatment with andrographolide. RESULT(S): The constitutive NF-κB DNA-binding activity and protein expression levels of p50 and p65, and mRNA and protein levels of COX-2, VEGF, and TF in cases were significantly higher than that of controls. The binding activity level correlated positively with dysmenorrhea severity in cases. The TNF-α stimulation further increased the binding activity, and the mRNA and protein levels of COX-2, VEGF, and TF, but treatment with andrographolide significantly reduced them. CONCLUSION(S): NF-κB may be a pivotal transcription factor involved in the development of adenomyosis. Targeting NF-κB with inhibitors, like andrographolide, may hold promises of treating adenomyosis.

My notes (saved in your browser only)

Condition tags

adenomyosis

MeSH descriptors

Adenomyosis Diterpenes NF-kappa B Tumor Necrosis Factor-alpha Adenomyosis Adenomyosis Adenomyosis Adult Adult Anti-Inflammatory Agents Anti-Inflammatory Agents Anti-Inflammatory Agents Case-Control Studies Case-Control Studies Cyclooxygenase 2 Cyclooxygenase 2 Cyclooxygenase 2 Cyclooxygenase 2 Diterpenes Diterpenes

Citation neighborhood (2-hop)

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. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (94)

Cited by (50)

Source provenance

europepmc
last seen: 2026-10-19T06:17:24.038039+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-10-08T21:11:59.585523+00:00
License: CC0 · commercial use OK