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Diallyl disulfide attenuates acetaminophen-induced renal injury in rats

机译:二烯丙基二硫化物减轻对乙酰氨基酚引起的大鼠肾脏损伤

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摘要

This study investigated the protective effects of diallyl disulfide (DADS) against acetaminophen (AAP)-induced acute renal injury in male rats. We also investigated the effects of DADS on kidney injury molecule-1 (KIM-1) and neutrophil gelatinase-associated lipocalin (NGAL), which are novel biomarkers of nephrotoxicity in renal tissues, in response to AAP treatment. The following four experimental groups were evaluated: (1) vehicle control, (2) AAP (1,000 mg/kg), (3) AAP&DADS, and (4) DADS (50 mg/kg/day). AAP treatment caused acute kidney injury evidenced by increased serum blood urea nitrogen (BUN) levels and histopathological alterations. Additionally, Western blot and immunohistochemistry analysis showed increased expression of KIM-1 and NGAL proteins in renal tissues of AAP-treated rats. In contrast, DADS pretreatment significantly attenuated the AAP-induced nephrotoxic effects, including serum BUN level and expression of KIM-1 and NGAL proteins. Histopathological studies confirmed the renoprotective effect of DADS. The results suggest that DADS prevents AAP-induced acute nephrotoxicity, and that KIM-1 and NGAL may be useful biomarkers for the detection and monitoring of acute kidney injury associated with AAP exposure.
机译:这项研究调查了二烯丙基二硫化物(DADS)对对乙酰氨基酚(AAP)诱导的雄性大鼠急性肾损伤的保护作用。我们还研究了DADS对肾脏损伤分子1(KIM-1)和中性白细胞明胶酶相关脂质钙蛋白(NGAL)的影响,这是肾脏组织中肾毒性的新生物标志物,以响应AAP治疗。评价了以下四个实验组:(1)媒介物对照组,(2)AAP(1,000 mg / kg),(3)AAP&DADS和(4)DADS(50 mg / kg / day)。 AAP治疗可导致急性肾损伤,其表现为血清血尿素氮(BUN)水平升高和组织病理学改变。此外,蛋白质印迹和免疫组织化学分析显示,在AAP治疗的大鼠的肾脏组织中,KIM-1和NGAL蛋白的表达增加。相反,DADS预处理显着减弱了AAP诱导的肾毒性作用,包括血清BUN水平以及KIM-1和NGAL蛋白的表达。组织病理学研究证实了DADS的肾脏保护作用。结果表明,DADS可以预防AAP引起的急性肾毒性,并且KIM-1和NGAL可能是用于检测和监测与AAP暴露相关的急性肾脏损伤的有用生物标志物。

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