Altinoz E, Oner Z, Elbe H, Cigremis Y, Turkoz Y
Department of Medical Biochemistry, Health High School, Karabuk University, Karabuk, Turkey
Department of Anatomy, Faculty of Medicine, Inonu University, Malatya, Turkey.
Hum Exp Toxicol. 2015 Feb;34(2):127-34. doi: 10.1177/0960327114538989. Epub 2014 Jun 12.
The reactive oxygen species take role in pathogenesis of many diseases including hypoxia, hypercholesterolemia, atherosclerosis, nephropathy, hypertension, ischemia-reperfusion damage, and heart defects. The aim of this study was to evaluate whether crocin administration could protect kidney injury from oxidative stress in streptozotocin-induced diabetic rats. The rats were randomly divided into 3 groups each containing 10 animals as follows: group 1, control group; group 2, diabetes mellitus (DM) group; and group 3, DM + crocin group. At the end of the study, trunk blood was collected to determine the plasma levels of blood urea nitrogen (BUN) and creatinine (Cr). The kidney tissue was removed, and biochemical and histological changes were examined. Diabetes caused a significant increase in malondialdehyde (MDA) and xanthine oxidase (XO) activities and a decrease in glutathione (GSH) contents (p < 0.01) when compared with control group in the rat kidneys. Crocin given to DM rats significantly decreased MDA (p < 0.01) and XO (p < 0.05) activities and elevated GSH (p < 0.05) contents when compared with DM group. Plasma levels of BUN and Cr were significantly higher in the DM group when compared with the control group (p < 0.01). Pretreatment of the DM animals with crocin decreased the high level of serum Cr and BUN. Control group was normal in histological appearance, but congestion, severe inflammation, tubular desquamation, tubular necrosis, and hydropic degeneration in tubular cells were observed in the DM group. Histopathological changes markedly reduced, and appearance of kidney was nearly similar to control group in DM + crocin group. Our results show that crocin could be beneficial in reducing diabetes-induced renal injury.
活性氧参与多种疾病的发病机制，包括缺氧、高胆固醇血症、动脉粥样硬化、肾病、高血压、缺血再灌注损伤和心脏缺陷。本研究的目的是评估给予西红花苷是否能保护链脲佐菌素诱导的糖尿病大鼠免受氧化应激所致的肾损伤。大鼠被随机分为3组，每组10只动物，分组如下：第1组，对照组；第2组，糖尿病（DM）组；第3组，DM+西红花苷组。在研究结束时，采集大鼠躯干血以测定血浆尿素氮（BUN）和肌酐（Cr）水平。取出肾脏组织，检查其生化和组织学变化。与对照组相比，糖尿病导致大鼠肾脏中丙二醛（MDA）和黄嘌呤氧化酶（XO）活性显著增加，谷胱甘肽（GSH）含量降低（p<0.01）。与DM组相比，给予DM大鼠西红花苷可显著降低MDA（p<0.01）和XO（p<0.05）活性，并提高GSH（p<0.05）含量。与对照组相比，DM组的血浆BUN和Cr水平显著更高（p<0.01）。用西红花苷预处理DM动物可降低血清Cr和BUN的高水平。对照组组织学外观正常，但DM组观察到充血、严重炎症、肾小管脱落、肾小管坏死和肾小管细胞水肿变性。在DM+西红花苷组中，组织病理学变化明显减轻，肾脏外观与对照组几乎相似。我们的结果表明，西红花苷可能有助于减轻糖尿病诱导的肾损伤。
