Immunopharmacology and immunotoxicology · 2025
Febuxostat attenuates cyclophosphamide-induced ovarian toxicity; role of TLR4/NFκB/NLRP3 signaling pathway in female wistar albino rats.
СтатьяНазвание и аннотация: Перевод в очереди
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Abdelzaher Walaa Yehia, Hassan Marwa, Abdel-Aziz Asmaa Mohamed, Abd Elghfar Mohamed Hassan M, Reda Sameh, Saleh Rabeh Khairy, Atta Medhat, Mohamed Abdelaleem Abdelnour, Elsayed Samar Hisham, Taghian Asmaa S, Khalaf Hanaa Mohamed
Аннотация
BACKGROUND: Our goal was to assess if febuxostat (FEB) could prevent ovarian damage caused by cyclophosphamide (CP).
MATERIAL AND METHODS: Four sets were created: control group, FEB group: received FEB 10 mg/kg orally for 14 days, CPgroup: a single ip dose of CP (200 mg/kg) at 8th day and CP+FEB group. Serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), anti-mullerian hormone (AMH), malondialdehyde (MDA), total antioxidant capacity (TAC), interluken-6 (IL-6), tumor necrosis factor alpha (TNF-α), Nod-like receptor protein 3 (NLRP3) were estimated. Apoptotic Bcl-2-associated protein x (Bax) and anti-apoptotic B-cell leukemia/lymphoma 2 protein (Bcl2) gene expression were measured. Histological alterations and immuno-expression of nuclear factor-kappa B (NF-κB) and toll like receptor4 (TLR4) were assessed.
RESULTS: FSH, LH, MDA, IL-6, TNF-α, NLRP3 levels, Bax and Bax/Bcl-2 ratio gene expression, NF-κB and TLR4 immuno-expression were all significantly elevated in the CP group. AMH, TAC levels and Bcl-2 gene expression have significantly decreased. Every metric indicated a notable improvement with FEB.
CONCLUSION: By controlling the TLR4/NF-Κb/NLRP3 signaling pathway, FEB has strong mitigating effects against oxidative stress, inflammatory processes, and apoptosis that result from CP-induced ovarian toxicity.
MATERIAL AND METHODS: Four sets were created: control group, FEB group: received FEB 10 mg/kg orally for 14 days, CPgroup: a single ip dose of CP (200 mg/kg) at 8th day and CP+FEB group. Serum follicle-stimulating hormone (FSH), luteinizing hormone (LH), anti-mullerian hormone (AMH), malondialdehyde (MDA), total antioxidant capacity (TAC), interluken-6 (IL-6), tumor necrosis factor alpha (TNF-α), Nod-like receptor protein 3 (NLRP3) were estimated. Apoptotic Bcl-2-associated protein x (Bax) and anti-apoptotic B-cell leukemia/lymphoma 2 protein (Bcl2) gene expression were measured. Histological alterations and immuno-expression of nuclear factor-kappa B (NF-κB) and toll like receptor4 (TLR4) were assessed.
RESULTS: FSH, LH, MDA, IL-6, TNF-α, NLRP3 levels, Bax and Bax/Bcl-2 ratio gene expression, NF-κB and TLR4 immuno-expression were all significantly elevated in the CP group. AMH, TAC levels and Bcl-2 gene expression have significantly decreased. Every metric indicated a notable improvement with FEB.
CONCLUSION: By controlling the TLR4/NF-Κb/NLRP3 signaling pathway, FEB has strong mitigating effects against oxidative stress, inflammatory processes, and apoptosis that result from CP-induced ovarian toxicity.