庆大霉素诱导肾病中 Na/K-ATPase、NHE3、NBC1、AQP1 和 OAT 的表达降低。
Decreased Expression of Na/K-ATPase, NHE3, NBC1, AQP1 and OAT in Gentamicin-induced Nephropathy.
机构信息
Department of Internal Medicine, Chonnam National University Medical School, Gwangju 501-757, Korea.
出版信息
Korean J Physiol Pharmacol. 2008 Dec;12(6):331-6. doi: 10.4196/kjpp.2008.12.6.331. Epub 2008 Dec 31.
The present study was aimed to determine whether there is an altered regulation of tubular transporters in gentamicin-induced nephropathy. Sprague-Dawley male rats (200~250 g) were subcutaneously injected with gentamicin (100 mg/kg per day) for 7 days, and the expression of tubular transporters was determined by immunoblotting and immunohistochemistry. The mRNA and protein expression of OAT was also determined. Gentamicin-treated rats exhibited significantly decreased creatinine clearance along with increased plasma creatinine levels. Accordingly, the fractional excretion of sodium increased. Urine volume was increased, while urine osmolality and free water reabsorption were decreased. Immunoblotting and immunohistochemistry revealed decreased expression of Na(+)/K(+)-ATPase, NHE3, NBC1, and AQP1 in the kidney of gentamicin-treated rats. The expression of OAT1 and OAT3 was also decreased. Gentamicin-induced nephropathy may at least in part be causally related with a decreased expression of Na(+)/K(+)-ATPase, NHE3, NBC1, AQP1 and OAT.
本研究旨在探讨庆大霉素诱导的肾病中肾小管转运蛋白的调节是否发生改变。雄性 Sprague-Dawley 大鼠（200~250 g）皮下注射庆大霉素（100 mg/kg/天）7 天，通过免疫印迹和免疫组织化学测定肾小管转运蛋白的表达。还测定了 OAT 的 mRNA 和蛋白表达。庆大霉素处理的大鼠表现出肌酐清除率显著降低，同时血浆肌酐水平升高。相应地，钠的分数排泄增加。尿量增加，而尿渗透压和游离水重吸收减少。免疫印迹和免疫组织化学显示，庆大霉素处理的大鼠肾脏中 Na(+)/K(+)-ATP 酶、NHE3、NBC1 和 AQP1 的表达减少。OAT1 和 OAT3 的表达也减少。庆大霉素诱导的肾病至少部分可能与 Na(+)/K(+)-ATP 酶、NHE3、NBC1、AQP1 和 OAT 的表达减少有关。
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