The Suppression Effect of Kebar Extract on Endometriosis Lesion MDA and TNF -a Independent to VEGF A Study in Endometriosis Mice Mode
Kebar grass extract decreased MDA serum levels and TNF-α expression, leading to smaller endometriotic lesions in mice without affecting VEGF expression.
One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works
This experimental study evaluated whether Kebar grass extract would affect oxidative stress (serum malondialdehyde), inflammation (TNF-α), VEGF expression, and the size of endometriotic lesions in a mouse endometriosis model, compared with an untreated control and leuprolide acetate treatment. Twenty-one mice were assigned to three groups (control, leuprolide 1 mg/kg single dose, or Kebar extract 3 mg/day for 14 days), with outcomes measured by spectrophotometry for MDA, immunohistochemistry using immunoreactive scoring for TNF-α and VEGF, and computerized tracing for lesion area. Kebar extract significantly reduced MDA and lowered TNF-α expression and was associated with smaller lesion extension, but VEGF expression did not differ significantly between groups. The paper explicitly reports that the VEGF pathway was not affected, limiting conclusions to TNF-α/inflammation and oxidative-stress mechanisms rather than angiogenesis via VEGF in this model. This paper is centrally about endometriosis — it tests Kebar grass extract effects on oxidative stress, TNF-α, VEGF, and endometriotic lesion size in endometriosis mice.
Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works
Abstract
Full text
2,929 characters
· extracted from
oa-doi-fallback
· 6 sections
· click to expand
Background
Objective
Methods
Results
Conclusion
Keywords
Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.
My notes (saved in your browser only)
Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works
Condition tags
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 (23)
- Advances in the management of endometriosis: an update for clinicians via openalex
- Angiogenesis and Endometriosis via openalex
- Apoptosis and endometriosis via openalex
- Changes in tissue inflammation, angiogenesis and apoptosis in endometriosis, adenomyosis and uterine myoma after GnRH agonist therapy via openalex
- Comparison of Ovarial Malondialdehyde (MDA) Level between Endometriosis Rat Given with and without Curcumine Supplementation via openalex
- Endometriosis and Oxidative Stress via openalex
- Oxidative Stress and the Pathogenesis of Endometriosis via openalex
- Role of angiogenesis in endometriosis via openalex
- Role of oxidative stress in endometriosis via openalex
- Theories on the Pathogenesis of Endometriosis via openalex
- [TNF-alpha serum levels in women with endometriosis: prospective clinical study]. via openalex
- Vitamin C is effective for the prevention and regression of endometriotic implants in an experimentally induced rat model of endometriosis via openalex
- W7056790001 via openalex
- W1913115502 via openalex
- W1992634825 via openalex
- W2015293545 via openalex
- W2061164005 via openalex
- W2101356627 via openalex
- W2109540355 via openalex
- W2168801847 via openalex
- W6653017088 via openalex
- W6843361325 via openalex
- W1907235146 via openalex
Source provenance
- openalex
- last seen: 2026-06-04T00:00:01.174412+00:00