Sulfasalazine-induced renal injury in rats and the protective role of thiol-reductants
Sulfasalazine-induced renal injury in rats and the protective role of thiol-reductants
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DOI：
10.3109/0886022x.2015.1096731
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发表时间：
2016-01-02
期刊：
影响因子：
3
通讯作者：
Najibi, Asma
中科院分区：
文献类型：
--
作者：
Heidari, Reza;Taheri, Vahid;Najibi, Asma
磺胺吡啶广泛应用于人类炎症性疾病。肾损害是伴随柳氮磺胺嘧啶使用的严重不良反应。到目前为止，还没有针对这种并发症的特定治疗方案。氧化应激似乎在柳氮磺胺引起的肾损伤中起作用。本研究旨在探讨n -乙酰半胱氨酸（NAC）和二硫代苏糖醇（DTT）作为硫醇还原剂对磺胺嘧啶所致大鼠肾损伤的影响。经血清肌酐、尿素氮水平升高判断，连续14天口服柳氮磺胺吡啶（600mg/kg）可引起肾损伤。此外，给药后肾组织中活性氧和脂质过氧化水平升高。此外，还发现肾谷胱甘肽储存库在磺胺嘧啶处理的动物显著枯竭。药物治疗大鼠肾移植性脏器损伤的组织病理学检查。每日腹腔注射NAC（250和500mg/kg/天）和/或DTT（15和30mg/kg/天）可有效减轻磺胺吡啶所致肾损害。数据表明，巯基还原剂可以作为潜在的保护剂，治疗磺胺氮嗪对肾脏的不良反应。
Sulfasalazine is widely used for inflammatory-mediated disorders in human. Renal damage is a serious adverse effect accompanied sulfasalazine administration. No specific therapeutic option is available against this complication so far. Oxidative stress seems to play a role in sulfasalazine-induced renal injury. Current investigation was designed to evaluate the effect of N-acetyl cysteine (NAC) and dithiothreitol (DTT) as thiol reductants against sulfasalazine-induced renal injury in rats. Oral administration of sulfasalazine (600mg/kg for 14 consecutive days) caused renal injury as judged by increase in serum level of creatinine and blood urea nitrogen. Furthermore, the level of reactive oxygen species and lipid peroxidation were raised in kidney tissue after sulfasalazine administration. Additionally, it was also found that renal glutathione reservoirs were significantly depleted in sulfasalazine-treated animals. Histopathological examination of kidney endorsed organ injury in drug-treated rats. Daily intraperitoneal administration of NAC (250 and 500mg/kg/day) and/or DTT (15 and 30mg/kg/day) effectively alleviated renal damage induced by sulfasalazine. Data suggested that thiol reductants could serve as potential protective agents with therapeutic capabilities against sulfasalazine adverse effect toward kidney.