Experimental modeling, prevention, and treatment of endometriosis-associated adhesion formation in NIH/3T3 fibroblast cell line using bovhyaluronidase azoximer (in vitro)

L.V. Adamyan, L.G. Pivazyan, K.S. Mailova, Iuliia O. Peshkova, A.A. Stepanian
In: Russian Journal of Human Reproduction · 2024 · vol. 30(6) , pp. 61 · doi:10.17116/repro20243006161 · W4405869579
article OA: closed CC0 ⤵ 3 in-corpus citations
View on OpenAlex View at publisher
⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

Bovhyaluronidase azoximer was evaluated in an in vitro cell model, where it inhibited key profibrotic mechanisms including collagen I expression, metabolic activity, and myofibroblast migration, demonstrating antifibrotic potential for endometriosis-associated adhesion prevention and treatment.

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

⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

The paper investigates, in vitro using NIH/3T3 fibroblasts, whether bovhyaluronidase azoximer can prevent and treat endometriosis-associated adhesion/fibrosis-like changes induced by TGF-β1, assessing fibroblast phenotypes after 24-hour co-incubation (prevention) and the effect of the agent on activation of already differentiated myofibroblasts (treatment). It builds on the profibrotic role of TGF-β1 and the HA (hyaluronic acid)/CD44 axis in promoting fibroblast-to-myofibroblast transition, including α-SMA and collagen-related remodeling, and tests bovhyaluronidase azoximer as an intervention targeting this HA-related pathway. The main limitation explicitly implied by the study design is that findings are restricted to a cell culture system and cannot capture organism-level metabolism or inflammatory/immune interactions. This paper is centrally about endometriosis — it experimentally models endometriosis-associated adhesion formation and evaluates bovhyaluronidase azoximer’s antifibrotic/prophylactic and therapeutic effects in a TGF-β1-driven in vitro system.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Endometriosis is a gynecological disease characterized by the presence of tissue that is morphologically and functionally similar to the endometrium, but located outside the uterine cavity, with a chronic and recurrent course. According to literature, endometriosis affects approximately 10% of women of reproductive age worldwide. Fibrosis plays a key role in both the pathogenesis and progression of endometriosis, as well as in the manifestation of its symptoms. The fibrotic process is initiated by inflammation, which is accompanied by the release of cytokines, such as TGF-β1, IL-17, and others, leading to the activation of fibroblasts and their transformation into myofibroblasts. Myofibroblasts contribute to the excessive production of collagen, hyaluronic acid, and other components of the extracellular matrix, resulting in the formation of fibrous tissue and adhesions. This mechanism underlies the progression of endometriosis-associated adhesion processes, exacerbating the clinical picture of the disease, causing pain, dyspareunia, bleeding, organ dysfunction, infertility, and overall reduced quality of life. The study evaluated the effectiveness of bovhyaluronidase azoximer (an enzyme preparation that is a modified form of hyaluronidase, with azoximer being a biopolymer that enhances the pharmacological properties of hyaluronidase by increasing its stability and duration of action in the body) in both the prevention and treatment of endometriosis-associated adhesion processes. An in vitro cellular model was used for this purpose. Thus, in a cell model (in vitro), it was demonstrated that bovhyaluronidase azoximer inhibits key profibrotic mechanisms induced by transforming growth factor-β1 (TGF-β1), such as collagen I expression, metabolic activity, and myofibroblast migration, which confirms its antifibrotic potential. The application of bovhyaluronidase azoximer suppressed the metabolic activity and migration of myofibroblasts, confirming its antifibrotic potential. These results demonstrate promising prospects for the prevention and targeted therapy of fibrotic changes in endometriosis, as well as reducing the risk of adhesion formation, opening new possibilities for the comprehensive treatment of the disease.

My notes (saved in your browser only)

Condition tags

endometriosisdyspareuniainfertility

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 (64)

Cited by (3)

Source provenance

openalex
last seen: 2026-06-10T17:14:06.276822+00:00
unpaywall
last seen: 2026-06-02T02:00:03.124865+00:00
License: CC0 · commercial use OK