Department of Histology, Faculty of Medicine, Delta University for Science and Technology, Gamasa City, Mansoura, Egypt.
Yousef Abdullatif Jameel, Chair of Prophetic Medical Applications (YAJCPMA), Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia.
Oxid Med Cell Longev. 2020 Jul 20;2020:3295831. doi: 10.1155/2020/3295831. eCollection 2020.
The association between hypothyroidism and renal diseases has been described in many studies. was among the recently reported natural product that has the potential to prevent renal tissue damage and fibrosis. The aim of this study was to evaluate the possible protective effect of thymoquinone on the structure of the renal cortex of hypothyroid rats and explore the mechanism behind it.
An experimental model of hypothyroidism was induced in adult male Wistar rats by administration of propylthiouracil (6 mg/kg/body weight). One hypothyroid group was treated with thymoquinone at the dose of 50 mg/kg/body weight and compared to the untreated group. Thyroid function and oxidant/antioxidant status were assessed in the serum. Catalase gene expression was assessed using the real-time polymerase chain reaction. The kidney was assessed both histologically and immunohistochemically.
Administration of propylthiouracil resulted in a significant decrease in the serum levels of nitric oxide, reduced glutathione, and superoxide dismutase activity while the level of malondialdehyde significantly ( < 0.001) increased. Administration of thymoquinone alleviated this effect on the thyroid hormones and significantly increased the serum levels of antioxidants. Thymoquinone significantly ( < 0.001) upregulated catalase transcription by about 24-fold and could block the hypothyroidism-induced glomerular and tubular injury.
Thymoquinone may have a potential protective effect against hypothyroidism-induced renal injury acting through the attenuation of the oxidative stress and upregulation of renal catalase gene expression.
许多研究已经描述了甲状腺功能减退症与肾脏疾病之间的关联。 是最近报道的具有预防肾组织损伤和纤维化潜力的天然产物之一。本研究旨在评估胸腺醌对甲状腺功能减退症大鼠肾皮质结构的可能保护作用,并探讨其背后的机制。
通过给予丙硫氧嘧啶(6mg/kg/体重)在成年雄性 Wistar 大鼠中诱导甲状腺功能减退症的实验模型。一个甲状腺功能减退症组用 50mg/kg/体重的胸腺醌治疗,并与未治疗组进行比较。评估血清中的甲状腺功能和氧化应激/抗氧化状态。使用实时聚合酶链反应评估过氧化氢酶基因表达。对肾脏进行组织学和免疫组织化学评估。
丙硫氧嘧啶的给药导致血清中一氧化氮、还原型谷胱甘肽和超氧化物歧化酶活性显著降低,而丙二醛水平显著增加(<0.001)。胸腺醌的给药缓解了甲状腺激素的这种作用,并显著增加了抗氧化剂的血清水平。胸腺醌通过约 24 倍显著上调过氧化氢酶转录,并能阻断甲状腺功能减退症引起的肾小球和肾小管损伤。
胸腺醌可能通过减轻氧化应激和上调肾脏过氧化氢酶基因表达对甲状腺功能减退症引起的肾脏损伤具有潜在的保护作用。