ArticleInternational journal of reproductive biomedicine2026
Lesion size reduction in mouse model of endometriosis following clove (
Article in International journal of reproductive biomedicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Endometriosis affects about 10% of reproductive-age women, causing pelvic pain and infertility. Its progression involves angiogenesis and neurovascular innervation, mediated by vascular endothelial growth factor (VEGF) and brain-derived neurotrophic factor (BDNF). Clove leaf extract may suppress lesion growth by reducing these pathways through antioxidant and anti-inflammatory actions. Objective: This study evaluated clove leaf extract's impact on VEGF and BDNF pathways and lesion size in female mice with endometriosis, testing whether extract reduces VEGF, BDNF, and lesion area, with the hypothesis that intermediate dosage provides optimal efficacy. Materials and Methods: A total of 36 female BALB/c mouse endometriosis model (2-3 months old, weighing 20-30 gr) induced by uterine endometrial implantation with estrogen supplementation were randomly assigned to 4 groups: one untreated control group (K⁺) and 3 treatment groups receiving clove leaf extract at doses of 75 mg/kg-BW (P1), 150 mg/kg-BW (P2), and 300 mg/kg-BW (P3). Blood samples and peritoneal tissue were collected for analysis using commercial Enzyme-Linked Immunosorbent Assay kits targeting VEGF and BDNF, as well as Motic imaging for lesion assessment. Results: Following 14 days of clove leaf extract administration, endometriosis lesion area significantly decreased (p = 0.001), whereas VEGF (p = 0.27) and BDNF (p = 0.13) remained unchanged. Histological analysis corroborated lesion reduction, confirming extract's impact on lesion morphology without altering VEGF or BDNF. Conclusion: The hypothesized involvement of VEGF and BDNF was not supported by the data. The principal finding is a reduction in lesion size, with the underlying mechanism remaining uncertain and potentially independent of VEGF/BDNF modulation.
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