Karafakıoğlu Yasemin Sunucu, Bozkurt Mehmet Fatih, Hazman Ömer, Fıdan A Fatih
Department of Science Education, Faculty of Education, Uşak University, Uşak, Turkey
Department of Pathology, Faculty of Veterinary Medicine, University of Afyon Kocatepe, Afyonkarahisar, Turkey.
Biochem J. 2017 Mar 20;474(7):1195-1203. doi: 10.1042/BCJ20160971.
The aim of the present study was to investigate the effects of safranal on cisplatin-induced nephrotoxicity and oxidative stress in rats. Adult male Sprague-Dawley rats were randomly divided into five groups. The control group received physiological saline; animals in Group 2 received only safranal and in Group 3 received only cisplatin; 5 days of safranal treatment was performed following administration of cisplatin for the animals in Group 4; 5 days of safranal pretreatment was applied to the animals in Group 5 before administration of cisplatin. Cisplatin (7 mg/kg) was intraperitoneally injected as a single dose and safranal (200 mg/kg) was administered by gavage. Biochemical and histopathological methods were utilized for evaluation of the nephrotoxicity. The concentrations of creatinine and urea in plasma and levels of malondialdehyde (MDA) and glutathione (GSH) as well as total antioxidant status (TAS) and total oxidant status (TOS) were determined in kidney tissue. Administration of cisplatin to rats induced a marked renal failure, characterized with a significant increase in plasma creatinine and urea concentrations. MDA and TOS levels of rats that received cisplatin alone were not significantly different compared with those of the control group, but GSH and TAS levels in the only cisplatin-administered group were significantly decreased. Safranal administration produced amelioration in biochemical indices of nephrotoxicity in both plasma and kidney tissues when compared with the only cisplatin-administered group, pretreatment with safranal being more effective. As a result, safranal treatment might have a protective effect against cisplatin-induced nephrotoxicity and oxidative stress in rat.
本研究的目的是探讨藏红花醛对顺铂诱导的大鼠肾毒性和氧化应激的影响。成年雄性Sprague-Dawley大鼠被随机分为五组。对照组给予生理盐水；第2组动物仅给予藏红花醛，第3组仅给予顺铂；第4组动物在给予顺铂后进行5天的藏红花醛治疗；第5组动物在给予顺铂前进行5天的藏红花醛预处理。顺铂（7 mg/kg）以单剂量腹腔注射，藏红花醛（200 mg/kg）通过灌胃给药。采用生化和组织病理学方法评估肾毒性。测定肾组织中血浆肌酐和尿素浓度、丙二醛（MDA）和谷胱甘肽（GSH）水平以及总抗氧化状态（TAS）和总氧化状态（TOS）。给大鼠注射顺铂可导致明显的肾衰竭，其特征是血浆肌酐和尿素浓度显著升高。单独接受顺铂的大鼠的MDA和TOS水平与对照组相比无显著差异，但仅接受顺铂的组中的GSH和TAS水平显著降低。与仅接受顺铂的组相比，给予藏红花醛可改善血浆和肾组织中肾毒性的生化指标，藏红花醛预处理更有效。因此，藏红花醛治疗可能对顺铂诱导的大鼠肾毒性和氧化应激具有保护作用。
