Juniperus oxycedrus Extract Attenuates LPS-Associated Histological Injury and TRPV6/Inflammasome-Related Immunoreactivity in Rat Seminal Vesicles
LIFE, cilt.16, sa.11, ss.1-16, 2026 (Hakemli Dergi)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 16 Sayı: 11
- Basım Tarihi: 2026
- Dergi Adı: LIFE
- Derginin Tarandığı İndeksler: MLA - Modern Language Association Database, MLA International Bibliography
- Sayfa Sayıları: ss.1-16
- Van Yüzüncü Yıl Üniversitesi Adresli: Evet
Özet
The seminal vesicle supplies a major fraction of ejaculate, but its early tissue response to bacterial endotoxin is poorly characterized. We assessed histology, histochemistry, and relative immunoreactivity for TRPV6, CARD11, NLRP3, ASC, and total GSDMD following acute intravenous challenge with bacterial endotoxin (lipopolysaccharide [LPS] from Escherichia coli serotype O55:B5; 5 mg/kg over 4 h) and examined tissue-level modification by methanolic Juniperus oxycedrus (JO) extract. Fifty male Wistar rats were assigned to control, LPS, LPS + aspirin, LPS + JO100 mg/kg, or LPS + JO200 mg/kg groups; seven per group were randomly selected for tissue analysis (n = 35). LPS was associated with epithelial disorganization, a higher trichrome-positive matrix score, and increased DAB immunoreactivity. Post-treatment with aspirin and either JO dose reduced group-level scores relative to LPS. Pooled correlations largely reflected group separation; after group adjustment and Benjamini–Hochberg correction across 15 comparisons, no residual correlation remained significant. Because only two extract doses were evaluated within this post-exposure protocol, formal pharmacological dose–response kinetics could not be evaluated. JO treatment was therefore associated with attenuation of early LPS-related tissue and staining changes. Because run-specific staining-control performance could not be verified, and cleaved GSDMD,caspase-1 activity, cytokines, and TRPV6-mediated calcium flux were not assessed, the findings do not establish target-specific protein expression, inflammasome activation, pyroptosis, or a causal TRPV6-NLRP3 pathway.