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首页> 外文期刊>Archives of Toxicology >Protect effect of bicyclol on cisplatin-induced nephrotoxicity in mice
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Protect effect of bicyclol on cisplatin-induced nephrotoxicity in mice

机译：双环醇对顺铂诱导的小鼠肾毒性的保护作用

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This study investigated the protective effects of bicyclol against cisplatin-induced nephrotoxicity and the possible mechanisms in mice. Bicyclol (250 mg/kg, p.o., 5 days) showed significant protection as evidenced by the decrease of elevated serum creatine and blood urea nitrogen, and improvement of histopathological injury induced by cisplatin. The formation of kidney malondialdehyde with a concomitant reduction of reduced glutathione were also inhibited by bicyclol, while the activities of kidney superoxide dismutase, catalase and glutathione peroxidase were all increased, respectively. Bicyclol also inhibited the increase of kidney and serum nitric oxide induced by cisplatin. In addition, induction of induced nitric oxide synthase and nitrotyrosine were suppressed by bicyclol. Bicyclol suppressed cisplatin-induced extracelluar signal regulated kinases 1/2 and p38 mitogen-activated protein kinase activation in the kidney of mice. Results obtained demonstrate that bicyclol pre-administration can prevent the nephrotoxicity induced by cisplatin.
机译：这项研究调查了双环酚对顺铂诱导的肾毒性的保护作用及其在小鼠中的可能机制。双环醇（250 mg / kg，口服，5天）显示出显着的保护作用，血清肌酸和血尿素氮升高的减少以及顺铂引起的组织病理学损伤的改善证明了这一点。肾丙二醛的形成同时减少了谷胱甘肽的还原，双环也被抑制，而肾脏超氧化物歧化酶，过氧化氢酶和谷胱甘肽过氧化物酶的活性分别增加。双环醇还抑制顺铂诱导的肾脏和血清一氧化氮的增加。另外，双环醇抑制了诱导型一氧化氮合酶和硝基酪氨酸的诱导。双环醇抑制了小鼠肾脏中顺铂诱导的细胞外信号调节激酶1/2和p38丝裂原活化蛋白激酶的活化。获得的结果表明，双环醇的预先给药可以预防顺铂诱导的肾毒性。

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