Santi A, Baldissareli J, Murussi C R, Dias G R M, de Menezes C C, Zanini D, Abdalla F H, Thomé G R, Martins C C, Schetinger M R C, Loro V L
Departamento de Química, Centro de Ciências Naturais e Exatas, Programa de Pós-Graduação em Ciências Biológicas: Bioquímica Toxicológica, Universidade Federal de Santa Maria, RS, Brazil.
Exp Clin Endocrinol Diabetes. 2014 Oct;122(9):533-9. doi: 10.1055/s-0034-1376968. Epub 2014 Jun 11.
The objective of the present study was to evaluate the effect of quercetin on oxidative stress biomarkers in methimazole (MMI) - induced hypothyroidism male rats. Hypothyroidism was induced by administering MMI at 20 mg/100 ml in the drinking water, for 1 month. After achieved hypothyroidism, rats received orally 10 or 25 mg/kg of quercetin (QT) for 8 weeks. 60 male wistar rats were randomly divided into 6 groups (group I, control; group II, QT10; group III, QT25; group IV, hypothyroid; group V, hypothyroid+QT10; group VI, hypothyroid+QT25). Liver, kidney and serum TBARS levels significantly increased in hypothyroid rats when compared to controls, along with increased protein carbonyl (PCO) in liver and increased ROS levels in liver and kidney tissues. QT10 and QT25 were effective in decreasing TBARS levels in serum and kidney, PCO levels in liver and ROS generation in liver and kidney. MMI - induced hypothyroidism also increased TBARS levels in cerebral cortex and hippocampus that in turn were decreased in rats treated with QT25. Moreover, the administration of QT25 to hypothyroid rats resulted in decreased SOD activities in liver and whole blood and increased liver CAT activity. Liver and kidney ascorbic acid levels were restored with quercetin supplementation at both concentrations. QT10 and QT25 also significantly increased total oxidative scavenging capacity in liver and kidney tissues from hypothyroid rats. These findings suggest that MMI - induced hypothyroidism increases oxidative stress parameters and quercetin administration could exert beneficial effects against redox imbalance in hypothyroid status.
本研究的目的是评估槲皮素对甲巯咪唑（MMI）诱导的甲状腺功能减退雄性大鼠氧化应激生物标志物的影响。通过在饮水中给予20mg/100ml的MMI诱导甲状腺功能减退1个月。甲状腺功能减退形成后，大鼠口服10或25mg/kg的槲皮素（QT），持续8周。将60只雄性Wistar大鼠随机分为6组（I组，对照组；II组，QT10组；III组，QT25组；IV组，甲状腺功能减退组；V组，甲状腺功能减退+QT10组；VI组，甲状腺功能减退+QT25组）。与对照组相比，甲状腺功能减退大鼠的肝脏、肾脏和血清丙二醛水平显著升高，同时肝脏中的蛋白质羰基（PCO）增加，肝脏和肾脏组织中的活性氧水平升高。QT10和QT25可有效降低血清和肾脏中的丙二醛水平、肝脏中的PCO水平以及肝脏和肾脏中的活性氧生成。MMI诱导的甲状腺功能减退还会增加大脑皮层和海马体中的丙二醛水平，而在接受QT25治疗的大鼠中，这一水平会降低。此外，给甲状腺功能减退大鼠施用QT25会导致肝脏和全血中的超氧化物歧化酶活性降低，肝脏中的过氧化氢酶活性增加。补充两种浓度的槲皮素均可恢复肝脏和肾脏中的抗坏血酸水平。QT10和QT25还显著提高了甲状腺功能减退大鼠肝脏和肾脏组织中的总氧化清除能力。这些发现表明，MMI诱导的甲状腺功能减退会增加氧化应激参数，而施用槲皮素可以对甲状腺功能减退状态下的氧化还原失衡发挥有益作用。
