Effects of bromelain on endocannabinoid system and oxidative stress in a rat model of endometriosis
Revista da Associacao Medica Brasileira, cilt.72, sa.8, 2026 (SCI-Expanded, Scopus)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 72 Sayı: 8
- Basım Tarihi: 2026
- Doi Numarası: 10.1590/1806-9282.20260396
- Dergi Adı: Revista da Associacao Medica Brasileira
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, EMBASE, MEDLINE
- Anahtar Kelimeler: Bromelain, Endocannabinoids, Endometriosis, Oxidative stress
- Açık Arşiv Koleksiyonu: AVESİS Açık Erişim Koleksiyonu
- Yozgat Bozok Üniversitesi Adresli: Evet
Özet
OBJECTIVE: The objective of this study is to evaluate the effects of bromelain on serum endocannabinoid levels and oxidative stress markers in a rat model of surgically induced endometriosis. METHODS: A total of 24 female Wistar albino rats were randomly assigned to three groups (n=8 each): Sham, endometriosis, and endometriosis treated with bromelain (endometriosis+B). Endometriosis was induced by autotransplantation of uterine tissue. Bromelain (20 mg/kg/day) was administered orally for 15 consecutive days. Serum levels of 2-arachidonoylglycerol, anandamide, superoxide dismutase, glutathione, and malondialdehyde were measured using ELISA. Statistical analysis was performed using one-way analysis of variance followed by Tukey’s post hoc test. RESULTS: Induction of endometriosis significantly reduced serum 2-arachidonoylglycerol, anandamide, superoxide dismutase, and glutathione levels while increasing malondialdehyde concentrations compared with the Sham group (p<0.05). Bromelain treatment significantly improved most endocannabinoid and oxidative stress parameters compared with the untreated endometriosis group (p<0.05). CONCLUSION: Bromelain ameliorated endocannabinoid deficiency and oxidative stress in experimental endometriosis. These findings suggest that bromelain may represent a promising non-hormonal therapeutic candidate targeting interconnected inflammatory and redox pathways in endometriosis.