因應(yīng)用不當(dāng)或飲食污染攝入馬兜鈴酸I所引起的、以進(jìn)展性間質(zhì)纖維化為特征的急慢性腎炎稱(chēng)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(duì)腎臟其他組織細(xì)胞未表現(xiàn)出明顯的直接損傷作用。因此,近曲小管上皮細(xì)胞通過(guò)有機(jī)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(lái)對(duì)腎小管攝取馬兜鈴酸I的機(jī)制已明確,但參與其在腎小管上皮細(xì)胞頂膜側(cè)轉(zhuǎn)運(yùn)的蛋白鮮有報(bào)道。通過(guò)綜述馬兜鈴酸I在腎小管的消除機(jī)制,以期為預(yù)防和治療馬兜鈴酸腎病提供新靶點(diǎn)。

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(xué)特色重點(diǎn)實(shí)驗(yàn)室項(xiàng)目(黔教合KY字[2021]004); 貴州省科技廳基礎(chǔ)研究計(jì)劃資助項(xiàng)目(黔科合基礎(chǔ)-ZK[2022]一般465)