Protective effects of fisetin on ovarian ischemia-reperfusion injury in rats via modulation of the TLR4-MyD88-TRAF6 signaling pathway.

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Acta cirurgica brasileira Pub Date : 2025-09-19 eCollection Date: 2025-01-01 DOI:10.1590/acb405925

Qianqian Gao, Dan Zhao, Wencong He

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Abstract

Purpose: To investigate the protective effects of fisetin on ovarian ischemia-reperfusion injury in rats, focusing on the modulation of the TLR4-MyD88-TRAF6 signaling pathway.

Methods: Wistar rats randomly divided into different groups received oral administration of fisetin (5, 10 and 15 mg/kg). Body weight and ovary weight were measured. Hormones, hematological, antioxidant, cytokines, inflammatory and apoptosis parameters were assessed. Histological and histopathologic evaluations were conducted on ovary tissue. Different mRNA expressions were estimated.

Results: Dose dependent treatment significantly improved body and ovary weight along with alteration in hematological parameters such as red blood cells, white blood cells, hemoglobin, platelet, lymphocyte; antioxidant parameters, including malonaldehyde, superoxide dismutase, glutathione, glutathione peroxidase, catalase; cytokines viz., tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6), interleukin-10 (IL-10), interleukin-18 (IL-18); inflammatory parameters such as cyclooxynase-2, inducible nitric oxide synthetase (iNOS), prostaglaindin, nuclear kappa B factor (NF-κB), C reactive protein and apoptosis parameters, including Bcl-2, Bax, and caspase-3. Fisetin treatment significantly (p < 0.001) altered the mRNA expression of TNF-α, IL-6, IL-1β, IL-10, Bax, Bcl-2, caspase-3, toll-like receptor 4, myeloid differentiation primary response protein 88, tumor necrosis factor receptor-associated factor 6, endothelial nitric oxide synthase, iNOS, NF-κB, inhibitor of kappaB kinase alpha, heme oxygenase-1, and nuclear factor erythroid 2-related factor 2. Fisetin treatment altered the hemorrhage, vascular proliferation, polymorphonuclear leukocyte, edema, vascular congestion, and apoptosis.

Conclusion: Fisetin ameliorated the ovary injury against ovarian ischemia-reperfusion via conquering TLR4-MyD88-TRAF6 signaling pathway.

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非西汀通过调节TLR4-MyD88-TRAF6信号通路对大鼠卵巢缺血再灌注损伤的保护作用。

目的：探讨非西汀对大鼠卵巢缺血再灌注损伤的保护作用，重点研究其对TLR4-MyD88-TRAF6信号通路的调节作用。方法：Wistar大鼠随机分为不同组，分别口服非瑟酮（5、10、15 mg/kg）。测定体重和卵巢重量。评估激素、血液学、抗氧化、细胞因子、炎症和凋亡参数。对卵巢组织进行组织学和组织病理学评价。估计不同mRNA的表达。结果：剂量依赖性治疗可显著改善体、卵巢重量，红细胞、白细胞、血红蛋白、血小板、淋巴细胞等血液学指标发生改变；抗氧化参数，包括丙二醛、超氧化物歧化酶、谷胱甘肽、谷胱甘肽过氧化物酶、过氧化氢酶；细胞因子：肿瘤坏死因子-α (TNF-α)、白细胞介素-1β (IL-1β)、白细胞介素-6 （IL-6）、白细胞介素-10 （IL-10）、白细胞介素-18 (IL-18)；炎症参数如环氧化酶-2、诱导型一氧化氮合成酶（iNOS）、前列腺素、核κB因子（NF-κB）、C反应蛋白和凋亡参数如Bcl-2、Bax和caspase-3。非西汀治疗显著（p < 0.001）改变了TNF-α、IL-6、IL-1β、IL-10、Bax、Bcl-2、caspase-3、toll样受体4、髓样分化原发性反应蛋白88、肿瘤坏死因子受体相关因子6、内皮型一氧化氮合酶、iNOS、NF-κB、kappaB激酶α抑制剂、血红素加氧酶1、核因子红细胞2相关因子2的mRNA表达。非西汀治疗改变了出血、血管增殖、多形核白细胞、水肿、血管充血和细胞凋亡。结论：非西汀通过征服TLR4-MyD88-TRAF6信号通路改善卵巢缺血再灌注损伤。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Acta cirurgica brasileira

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