Tunçdemir M, Ertürküner S P, Özçelik D
1 Department of Medical Biology, Cerrahpasa Faculty of Medicine, Istanbul University, Istanbul, Turkey.
2 Department of Histology and Embryology, Cerrahpasa Faculty of Medicine, Istanbul University, Istanbul, Turkey.
Hum Exp Toxicol. 2017 Aug;36(8):813-822. doi: 10.1177/0960327116666619. Epub 2016 Sep 7.
Several mechanisms for the pathogenesis of diabetic complications have been proposed, one of which is abnormal zinc (Zn) homeostasis. Zn is necessary for proper liver function since it has important antioxidant, anti-inflammatory, and antiapoptotic properties. We aimed to investigate whether or not Zn has morphologically protective effect on diabetes-induced liver damage in rats. In addition, we have investigated the role of Zn supplementation on apoptosis, lipid peroxidation levels, and the distribution of metallothionein (MT) in diabetic liver tissue. Wistar albino rats were divided into four groups: control, Zn, diabetic, and Zn-diabetic group. Experimental diabetes was induced by a single-dose streptozotocin intraperitoneally and Zn was administrated via gastric gavage tube for 6 weeks. MT expressions were showed with immunohistochemical staining and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay was used for apoptosis. Also, Zn, MT, and malondialdehyde (MDA) levels were determined in liver of rats. MDA levels of the Zn-supplemented diabetic group was less than the diabetic group though MT levels were increased. The number of apoptotic cells per unit area was found to be significantly decreased in this group. In the Zn-supplemented diabetic group, fibrotic tissue density and the collagen tissue density were observed less than the diabetic group. MT immunoreactivity was observed less in Zn-supplemented diabetic group. In conculusion, the present study indicated that Zn has a potential in preventing or even repairing effect against diabetic damage of the liver cells by increasing expression of MT and by reducing the apoptotic cell death and the oxidative stress.
糖尿病并发症发病机制的几种机制已被提出，其中之一是锌（Zn）稳态异常。锌对肝脏正常功能至关重要，因为它具有重要的抗氧化、抗炎和抗凋亡特性。我们旨在研究锌对糖尿病诱导的大鼠肝脏损伤是否具有形态学保护作用。此外，我们还研究了补充锌对糖尿病肝脏组织中细胞凋亡、脂质过氧化水平和金属硫蛋白（MT）分布的作用。将Wistar白化大鼠分为四组：对照组、锌组、糖尿病组和锌 - 糖尿病组。通过腹腔注射单剂量链脲佐菌素诱导实验性糖尿病，并通过胃管给予锌6周。用免疫组织化学染色显示MT表达，并用末端脱氧核苷酸转移酶介导的dUTP缺口末端标记法检测细胞凋亡。此外，还测定了大鼠肝脏中的锌、MT和丙二醛（MDA）水平。补充锌的糖尿病组的MDA水平低于糖尿病组，尽管MT水平有所升高。发现该组每单位面积的凋亡细胞数量显著减少。在补充锌的糖尿病组中，观察到纤维化组织密度和胶原组织密度低于糖尿病组。补充锌的糖尿病组中MT免疫反应性较低。总之，本研究表明，锌通过增加MT表达、减少凋亡细胞死亡和氧化应激，对预防甚至修复肝细胞的糖尿病损伤具有潜在作用。
