Taslidere E, Gul M, Elbe H, Cetin A, Vardi N, Ozyalin F, Turkoz Y
Bratisl Lek Listy. 2016;117(5):276-82. doi: 10.4149/bll_2016_054.
The aim of the present study was to clarify the role of oxidative stress in streptozotocin induced liver injury and the possible protective effect of caffeic acid phenethyl ester (CAPE) using histological and biochemical parameters. 32 male Wistar rats were divided into 4 groups as follows: Group 1: Control animals, Group 2: Control animals given CAPE Group 3: STZ-induced diabetic animals (DM group), Group 4: STZ-induced diabetic rats given CAPE (DM+CAPE group). All the injections started on the same day of single-dose STZ injection and continued for 20 days. At the end of this period, livers were removed and processed for routine histological procedures. Biochemical parameters and morphological changes were examined. In DM group, blood glucose levels were significantly increased compared with the control group. Significant increases in tissue malondialdehyde (MDA) level and decreases in superoxide dismutase (SOD) and total glutathione (GSH) activities were detected in DM group. Administration of CAPE significantly reduced these values. STZ-induced histopathological alterations including inflammatory cell infiltration around portal triad, congestion, loss of glycogen in the hepatocytes. Additionally, degenerative cellular alterations, such as numerous vacuolizations including myelinic figure formation, pyknotic nuclei with peripheral localization of heterochromatin condensation and mitochondrial elongation were observed in cytoplasm of hepatocytes. CAPE significantly reduced these histopathological changes. Our results indicate that CAPE should be considered in the prevention of oxidative stress in diabetic liver.
本研究的目的是利用组织学和生化参数阐明氧化应激在链脲佐菌素诱导的肝损伤中的作用以及咖啡酸苯乙酯（CAPE）可能的保护作用。将32只雄性Wistar大鼠分为以下4组：第1组：对照动物；第2组：给予CAPE的对照动物；第3组：链脲佐菌素诱导的糖尿病动物（糖尿病组）；第4组：给予CAPE的链脲佐菌素诱导的糖尿病大鼠（糖尿病+CAPE组）。所有注射均在单剂量链脲佐菌素注射的同一天开始，并持续20天。在此期间结束时，取出肝脏并进行常规组织学处理。检查生化参数和形态学变化。在糖尿病组中，血糖水平与对照组相比显著升高。在糖尿病组中检测到组织丙二醛（MDA）水平显著升高，超氧化物歧化酶（SOD）和总谷胱甘肽（GSH）活性降低。给予CAPE可显著降低这些值。链脲佐菌素诱导的组织病理学改变包括门管区周围的炎性细胞浸润、充血、肝细胞糖原丢失。此外，在肝细胞胞质中观察到退行性细胞改变，如包括髓鞘样结构形成的大量空泡化、异染色质凝聚外周定位的固缩核和线粒体延长。CAPE显著减轻了这些组织病理学变化。我们的结果表明，在预防糖尿病性肝氧化应激方面应考虑使用CAPE。
