因應用不當或飲食污染攝入馬兜鈴酸I所引起的、以進展性間質(zhì)纖維化為特征的急慢性腎炎稱為馬兜鈴酸腎病或巴爾干地方性腎病。馬兜鈴酸I特異性損傷近端小管,而對腎臟其他組織細胞未表現(xiàn)出明顯的直接損傷作用。因此,近曲小管上皮細胞通過有機陰離子蛋白1和3特異性攝入馬兜鈴酸I,是馬兜鈴酸I發(fā)揮特異性腎毒性作用的關(guān)鍵。近年來對腎小管攝取馬兜鈴酸I的機制已明確,但參與其在腎小管上皮細胞頂膜側(cè)轉(zhuǎn)運的蛋白鮮有報道。通過綜述馬兜鈴酸I在腎小管的消除機制,以期為預防和治療馬兜鈴酸腎病提供新靶點。

Acute and chronic nephritis characterised by progressive interstitial fibrosis caused by ingestion of aristolochic acid I through 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.

R969.1，R969.3

貴州省法醫(yī)中藥毒理學特色重點實驗室項目(黔教合KY字[2021]004); 貴州省科技廳基礎(chǔ)研究計劃資助項目(黔科合基礎(chǔ)-ZK[2022]一般465)