Dihydroartemisinin attenuates ischemia/reperfusion-induced renal tubular senescence by activating autophagy.
10.1016/S1875-5364(23)60398-X
- Author:
Huiling LIU
1
;
Zhou HUANG
1
;
Hong JIANG
1
;
Ke SU
2
;
Zilin SI
1
;
Wenhui WU
1
;
Hanyu WANG
1
;
Dongxue LI
1
;
Ninghua TAN
3
;
Zhihao ZHANG
4
Author Information
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.
3. State Key Laboratory of Natural Medicines, Department of TCMs Pharmaceuticals, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 211198, China. Electronic address: nhtan@cpu.edu.cn.
4. State Key Laboratory of Natural Medicines, Department of TCMs Pharmaceuticals, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 211198, China. Electronic address: 1620174425@cpu.edu.cn.
- Publication Type:Journal Article
- Keywords:
AKI;
Autophagy;
Dihydroartemisinin;
Fibrosis;
Renal tubular senescence
- MeSH:
Animals;
Kidney;
Acute Kidney Injury/chemically induced*;
Ischemia;
Reperfusion Injury/drug therapy*;
Autophagy;
Reperfusion
- From:
Chinese Journal of Natural Medicines (English Ed.)
2023;21(9):682-693
- CountryChina
- Language:English
-
Abstract:
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.
