首页|肾小管上皮细胞特异性转运马兜铃酸机制研究进展

肾小管上皮细胞特异性转运马兜铃酸机制研究进展

扫码查看
因应用不当或饮食污染摄入马兜铃酸Ⅰ所引起的、以进展性间质纤维化为特征的急慢性肾炎称为马兜铃酸肾病或巴尔干地方性肾病.马兜铃酸Ⅰ特异性损伤近端小管,而对肾脏其他组织细胞未表现出明显的直接损伤作用.因此,近曲小管上皮细胞通过有机阴离子蛋白1和3特异性摄入马兜铃酸Ⅰ,是马兜铃酸Ⅰ发挥特异性肾毒性作用的关键.近年来对肾小管摄取马兜铃酸Ⅰ的机制己明确,但参与其在肾小管上皮细胞顶膜侧转运的蛋白鲜有报道.通过综述马兜铃酸Ⅰ在肾小管的消除机制,以期为预防和治疗马兜铃酸肾病提供新靶点.
Advances in mechanism of specific transport of aristolochic acid in renal tubular epithelial cells
Acute and chronic nephritis characterised by progressive interstitial fibrosis caused by ingestion of aristolochic acid Ⅰthrough misapplication or dietary contamination is known as aristolochic acid nephropathy or Balkan endemic nephropathy.Aristolochic acid Ⅰ specifically damages the proximal tubules,while it does not show any significant direct damaging effect on other tissue cells of the kidney.Therefore,the specific uptake of aristolochic acid Ⅰ by proximal tubular epithelial cells via organic anionic proteins 1 and 3 is the key to the specific nephrotoxic effects of aristolochic acid Ⅰ.The mechanism of renal tubular uptake of aristolochic acid Ⅰ has been clarified in recent years,but the proteins involved in its transport on the apical side of renal tubular epithelial cells have rarely been reported.By reviewing the mechanism of aristolochic acid Ⅰ elimination in renal tubules,we hope to provide new targets for the prevention and treatment of aristolochic acid nephropathy.

aristolochic acidaristolochic acid Ⅰaristolochic acid nephropathyorganic anion transporternephrotoxicityproximal tubule

杨心怡、黄春华、李小芬、汤海明、楼迪栋

展开 >

贵州中医药大学基础医学院法医学教研室,贵州贵阳 550000

贵州省法医中药毒理学特色重点实验室,贵州贵阳 550000

贵州中医药大学司法鉴定所,贵州贵阳 550000

马兜铃酸 马兜铃酸Ⅰ 马兜铃酸肾病 有机阴离子转运蛋白 肾毒性 近端小管

贵州省法医中药毒理学特色重点实验室项目贵州省科技厅基础研究计划资助项目

黔教合KY字[2021]004黔科合基础-ZK[2022]一般465

2024

药物评价研究
天津药物研究院 中国药学会

药物评价研究

CSTPCD北大核心
影响因子:1.199
ISSN:1674-6376
年,卷(期):2024.47(2)
  • 53