Dihydroartemisinin attenuates ischemia/reperfusion-induced renal tubular senescence by activating autophagy  

作　　者：LIU Huiling HUANG Zhou JIANG Hong SU Ke SI Zilin WU Wenhui WANG Hanyu LI Dongxue TAN Ninghua ZHANG Zhihao 

机构地区：[1]State Key Laboratory of Natural Medicines,Department of TCMs Pharmaceuticals,School of Traditional Chinese Pharmacy,China Pharmaceutical University,Nanjing 211198,China [2]Department of Nephrology,Renmin Hospital of Wuhan University,Wuhan 430060,China

出　　处：《Chinese Journal of Natural Medicines》2023年第9期682-693,共12页中国天然药物（英文版）

基　　金：the National Natural Science Foundation of China(No.81700559);the Natural Science Foundation of Hubei Province(No.2021CFB360);the Program for Jiangsu Province Innovative Research Team.

摘　　要：Acute kidney injury(AKI)is an important factor for the occurrence and development of CKD.The protective effect of dihydroartemisinin on AKI and and reported mechanism have not been reported.In this study,we used two animal models including ischemia-reperfusion and UUO,as well as a high-glucose-stimulated HK-2 cell model,to evaluate the protective effect of dihydroartemisinin on premature senescence of renal tubular epithelial cells in vitro and in vivo.We demonstrated that dihydroartemisinin improved renal aging and renal injury by activating autophagy.In addition,we found that co-treatment with chloroquine,an autophagy inhibitor,abolished the anti-renal aging effect of dihydroartemisinin in vitro.These findings suggested that activation of autophagy/elimination of senescent cell might be a useful strategy to prevent AKI/UUO induced renal tubular senescence and fibrosis.

关 键 词：AKI DIHYDROARTEMISININ Renal tubular senescence Fibrosis AUTOPHAGY 

分 类 号：R965[医药卫生—药理学]