Kheiripour Nejat, Karimi Jamshid, Khodadadi Iraj, Tavilani Heidar, Goodarzi Mohammad Taghi, Hashemnia Mohammad
Department of Biochemistry, School of Medicine, Hamadan University of Medical Sciences, P.O. Box 65178-38736, Hamadan, Iran.
Department of Biochemistry, School of Medicine, Hamadan University of Medical Sciences, P.O. Box 65178-38736, Hamadan, Iran, Phone: +988138276293, Fax: +9881380208.
J Basic Clin Physiol Pharmacol. 2018 Jun 27;29(3):301-308. doi: 10.1515/jbcpp-2017-0122.
In this study, we have investigated whether silymarin intake influences lipid and glycogen content in conjunction with sirtuin1 (SIRT1) and sterol regulatory element-binding protein 1c (SREBP-1c) expressions in liver of type 2 diabetic rat.
Thirty-six male Wistar rats were randomly divided into six groups: control groups (C) and diabetic groups (D); the control groups received 60 or 120 mg/kg silymarin (C+S60 or C+S120), and the diabetic groups received 60 or 120 mg/kg silymarin (D+S60 or D+S120) daily for 8 weeks. Serum biochemical parameters, as well as glycogen, lipid and oxidative stress biomarkers, in the liver tissue were measured by spectrophotometric methods. Additionally, SIRT1 and SREBP-1c messenger RNA (mRNA) expressions were evaluated by quantitative polymerase chain reaction.
Diabetes caused a significantly increased fasting blood sugar, homeostasis model assessment for insulin resistance, liver total cholesterol and triglyceride (TG) content, which were attenuated after the administration of silymarin. Dietary silymarin caused the improvement of lipid content in the liver of diabetic rats. Moreover, silymarin administration promoted SIRT1, suppressed SREBP-1c mRNA expression, reduced liver nitric oxide and protein carbonyl content, and increased liver glycogen, catalase and glutathione peroxidase activity. Furthermore, histopathological changes were improved in the treated groups.
Silymarin administration considerably restored hepatic changes induced by streptozotocin and nicotinamide. The upregulation of SIRT1 mRNA expression by silymarin may be associated with decreased lipid, increased glycogen content and downregulation of the SREBP-1c gene in the liver.
在本研究中，我们调查了水飞蓟素的摄入是否会影响2型糖尿病大鼠肝脏中脂质和糖原含量，以及与沉默调节蛋白1（SIRT1）和固醇调节元件结合蛋白1c（SREBP-1c）表达的关系。
将36只雄性Wistar大鼠随机分为六组：对照组（C）和糖尿病组（D）；对照组每日分别给予60或120 mg/kg水飞蓟素（C+S60或C+S120），糖尿病组每日分别给予60或120 mg/kg水飞蓟素（D+S60或D+S120），持续8周。采用分光光度法测量血清生化参数以及肝组织中的糖原、脂质和氧化应激生物标志物。此外，通过定量聚合酶链反应评估SIRT1和SREBP-1c信使核糖核酸（mRNA）的表达。
糖尿病导致空腹血糖、胰岛素抵抗的稳态模型评估、肝脏总胆固醇和甘油三酯（TG）含量显著升高，给予水飞蓟素后这些指标有所减轻。饮食中的水飞蓟素可改善糖尿病大鼠肝脏中的脂质含量。此外，给予水飞蓟素可促进SIRT1表达，抑制SREBP-1c mRNA表达，降低肝脏一氧化氮和蛋白质羰基含量，并增加肝脏糖原、过氧化氢酶和谷胱甘肽过氧化物酶活性。此外，治疗组的组织病理学变化得到改善。
给予水飞蓟素可显著恢复链脲佐菌素和烟酰胺诱导的肝脏变化。水飞蓟素上调SIRT1 mRNA表达可能与肝脏脂质减少、糖原含量增加以及SREBP-1c基因下调有关。
