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首页> 外文期刊>Journal of biochemical and molecular toxicology >Nicorandil mitigates folic acid-induced nephrotoxicity in mice: Role of iNOS and eNOS
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Nicorandil mitigates folic acid-induced nephrotoxicity in mice: Role of iNOS and eNOS

机译：Nicorandil减轻小鼠的叶酸诱导的肾毒性：Inos和Enos的作用

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摘要

Folic acid (FA)-induced acute kidney injury (AKI) is a commonly used model in experimental animals for studying renal injury. This study aimed to investigate the probable protecting impact of nicorandil against FA-induced renal dysfunction. A mouse model was executed by a single injection of FA (250 mg/kg). Nicorandil was orally administrated in two doses (50 and 100 mg/kg) for 10 days. Nicorandil repressed the progression of FA-induced AKI as evidenced by the improvement of histopathological alterations and the substantial decrease of serum levels of crea-tinine, urea, blood urea nitrogen, malondialdehyde (MDA), and urinary protein levels. Moreover, nicorandil resulted in a profound reduction in oxidative stress as manifested by decreased MDA and increased reduced glutathione and superoxide dismutase in renal tissue. Notably, nicorandil suppressed FA-induced inflammation; it reduced renal levels of nuclear factor-κB, tumor necrosis factor-α, and interleukin-6. Furthermore, nicorandil decreased renal levels of nitric oxide, inducible nitric oxide synthase, and increased endothelial nitric oxide synthase. Lastly, nicorandil efficiently decreased expression of the proapoptotic protein (Bax) and caspase 3. Nicorandil confers dose-dependent protection against FA-induced AKI by alleviating oxidative stress, inflammation besides modulating nitric oxide synthase and reducing apoptosis.
机译：叶酸（FA）诱导的急性肾损伤（AKI）是研究肾损伤的常用实验动物模型。本研究旨在探讨尼可地尔对FA诱导的肾功能不全的可能保护作用。通过单次注射FA（250 mg/kg）建立小鼠模型。尼可地尔以两种剂量（50和100 mg/kg）口服10天。尼可地尔抑制了FA诱导的AKI的进展，其表现为组织病理学改变的改善以及血清克汀宁、尿素、血尿素氮、丙二醛（MDA）和尿蛋白水平的显著降低。此外，尼可地尔可显著降低氧化应激，表现为肾组织中MDA降低，还原型谷胱甘肽和超氧化物歧化酶增加。值得注意的是，尼可地尔抑制FA诱导的炎症；它降低了核因子-κB、肿瘤坏死因子-α和白细胞介素-6的肾脏水平。此外，尼可地尔降低了肾脏中一氧化氮、诱导型一氧化氮合酶的水平，并增加了内皮型一氧化氮合酶的水平。最后，尼可地尔有效降低促凋亡蛋白（Bax）和半胱氨酸天冬氨酸蛋白酶3的表达。尼可地尔通过减轻氧化应激、炎症以及调节一氧化氮合酶和减少细胞凋亡，对FA诱导的AKI具有剂量依赖性保护作用。

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