Department of Histology and Embryology, Ataturk University, Faculty of Medicine, 25240 Erzurum, Turkey.
J Mol Histol. 2011 Jun;42(3):273-87. doi: 10.1007/s10735-011-9331-9. Epub 2011 May 21.
The present study investigated whether diabetes worsened the onset of liver injury/damage during the ovariectomized (OVX)-induced postmenopausal period in rats. Diabetes results in severe complications in humans, such as liver failure. Estrogen and its derivatives are medically acceptable, powerful antioxidant agents that can enable liver and other important organs to defend themselves against oxidative related injury. Estrogen deficiency, which occurs in the postmenopausal period and in individuals with diabetes, may play a significant role in the progression of liver failure. In the present study, rats were divided into four groups: control (Group I), diabetic (Group II), ovariectomy (Group III) and ovariectomy plus diabetes (Group IV). After the experiments, quantitative histopathological and immunohistochemical changes in liver were detected using light microscopy and modern stereological systems. Histopathological examinations showed that there were many necrotic and apoptotic hepatocytes in the lobules of Group II. In addition, there were a larger number of necrotic cells in Group III than Group II. In contrast to Group II, there were also apoptotic cells in the portal areas in Group III. Moreover, evidence of liver injury was higher in the sections of Group IV compared with all other groups. In biochemical findings, there were statistically significant differences between all the groups (P < 0.001) for catalase (CAT), glutathione peroxidase (GSH) and myeloperoxidase (MPx) activity. In addition, the amount of lipid peroxidation (LPO) was significantly different between groups. In stereological results, there were significant differences between Groups I and II and Groups II and IV. The present study provided novel insight into the pernicious effects of ovariectomy on liver injury following the onset of diabetes. Indeed, the present study found that increases in liver oxidative activity in OVX rats following the onset of diabetes correlates with elevated MPx, LPO and histopathological changes in rat liver.
本研究旨在探讨糖尿病是否会加重去卵巢(OVX)诱导的绝经后大鼠肝损伤/损伤的发生。糖尿病会导致人类出现严重的并发症,如肝功能衰竭。雌激素及其衍生物是医学上可接受的、强大的抗氧化剂,可使肝脏和其他重要器官免受氧化相关损伤。绝经后和糖尿病患者中雌激素缺乏可能在肝功能衰竭的进展中起重要作用。在本研究中,大鼠分为四组:对照组(I 组)、糖尿病组(II 组)、去卵巢组(III 组)和去卵巢加糖尿病组(IV 组)。实验后,采用光镜和现代立体学系统检测肝的定量组织病理学和免疫组织化学变化。组织病理学检查显示,II 组肝小叶中有许多坏死和凋亡的肝细胞。此外,III 组的坏死细胞数量多于 II 组。与 II 组相比,III 组的门脉区也有凋亡细胞。此外,与所有其他组相比,IV 组的肝损伤证据更高。在生化发现方面,所有组之间 CAT、GSH 和 MPx 活性均存在统计学显著差异(P<0.001)。此外,各组之间的脂质过氧化(LPO)量也存在显著差异。在立体学结果中,I 组和 II 组以及 II 组和 IV 组之间存在显著差异。本研究为卵巢切除术后糖尿病发病时对肝损伤的有害影响提供了新的见解。事实上,本研究发现,糖尿病发生后 OVX 大鼠肝脏氧化活性的增加与 MPx、LPO 和大鼠肝脏的组织病理学变化升高相关。