アクティブボード・2017年5月
・・・・・2017年 5月 6日更新・・・・・
研究発表を行った学会;
第90回日本薬理学会年会
2017年 3月15日〜17日(長崎市)
タイトル;Involvement of Indoxyl sulfate in downregulation of pulmonary aquaporin-5 caused by acute kidney injury.
発表者;薮内 希実 氏
(熊本大学 薬学部 薬学科 臨床薬物動態学分野)
要旨;
High mortality of acute kidney injury (AKI) is associated with acute lung injury (ALI), which is a typical complication of AKI. Although dysregulation of lung salt and water channels following the AKI may play a pivotal role in ALI, the mechanism of its dysregulation remains unknown. Here, we examined involvement of indoxyl sulfate (IS), a typical uremic toxin, in dysregulation of pulmonary predominant water channel, aquaporin-5 (AQP-5), in bilateral nephrectomy (BNx)-induced AKI model. BNx evoked AKI with the increases in SCr, BUN, and serum IS levels, and exhibited thickening of interstitial tissue in the lung. Administration of AST-120, clinically used oral spherical adsorptive carbon beads, resulted in a significant decrease in serum IS level and thickening of interstitial tissue, which was accompanied with the decreases in IS accumulation in lung. In BNx rats, the significant decrease in pulmonary AQP-5 expression was observed. Moreover, administration of AST-120 markedly restore this downregulation of AQP-5 protein. These results suggest that BNx-induced AKI causes dysregulation of pulmonary AQP-5 expression, in which IS could play a toxico-physiological role as a mediator involved in renopulmonary crosstalk.