Department of Toxicology and Pharmacology, Nutrition Health Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
Department of Toxicology and Pharmacology, School of Pharmacy, Hamadan University of Medical Sciences, Hamadan, Iran.
J Biochem Mol Toxicol. 2022 Jul;36(7):e23063. doi: 10.1002/jbt.23063. Epub 2022 Apr 10.
This study was intended to assess the possible protective effect of resveratrol (Res) against oxidative stress and glucose hemostasis disorder in rats exposed to diazinon (DZN) for 4 weeks. Totally 25 Sprague-Dawley rats were divided randomly into five groups: Control (orally received corn oil), DZN group (orally received 70 mg/kg/day), and Res groups (received DZN 70 mg/kg/day plus Res doses of 5, 10, and 20 mg/kg bodyweight/-day), respectively. DZN significantly inhibited serum acetylcholinesterase enzyme (Ach E), serum and liver catalase, glutathione peroxidase activities, also total antioxidant capacities. On the other hand, DZN increased serum and liver malondialdehyde. DZN significantly increased Forkhead box protein O1 (Foxo1) expression and decreased phosphatase and tensin homolog (PTEN) and sirtuin 1 (Sirt-1) expression. DZN impaired glucose hemostasis. Instead, Res treatment significantly reversed status of oxidative stress and antioxidant enzymes activities induced by DZN. Also, Res improved glucose hemostasis. Res increased PTEN and Sirt-1 expression and reduced Foxo1 expression. Res administration ameliorated liver histopathological changes induced by DZN. These data confirmed that DZN significantly enhances oxidative stress and impairs glucose hemostasis. While Res showed a protective effect against the toxicity induced by DZN in rats.
本研究旨在评估白藜芦醇(Res)对连续 4 周接触二嗪磷(DZN)的大鼠氧化应激和血糖稳态紊乱的可能保护作用。总共 25 只 Sprague-Dawley 大鼠随机分为 5 组:对照组(口服玉米油)、DZN 组(口服 70mg/kg/天)和 Res 组(分别给予 DZN 70mg/kg/天加 Res 剂量 5、10 和 20mg/kg 体重/天)。DZN 显著抑制血清乙酰胆碱酯酶(AchE)、血清和肝脏过氧化氢酶、谷胱甘肽过氧化物酶活性,以及总抗氧化能力。另一方面,DZN 增加了血清和肝脏丙二醛的含量。DZN 显著增加叉头框蛋白 O1(Foxo1)的表达,降低磷酸酶和张力蛋白同源物(PTEN)和沉默调节蛋白 1(Sirt-1)的表达。DZN 损害了血糖稳态。相反,Res 治疗显著逆转了 DZN 诱导的氧化应激和抗氧化酶活性的状态。此外,Res 改善了血糖稳态。Res 增加了 PTEN 和 Sirt-1 的表达,降低了 Foxo1 的表达。Res 减轻了 DZN 引起的肝组织病理学变化。这些数据证实,DZN 显著增强了氧化应激并损害了血糖稳态。而 Res 对大鼠 DZN 毒性表现出保护作用。