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

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 di-hydroartemisinin on premature senescence of renal tubular epithelial cells in vitro and in vivo. We demonstrated that dihydroartemisin-in improved renal aging and renal injury by activating autophagy. In addition, we found that co-treatment with chloroquine, an auto-phagy inhibitor, abolished the anti-renal aging effect of dihydroartemisinin in vitro. These findings suggested that activation of auto-phagy/elimination of senescent cell might be a useful strategy to prevent AKI/UUO induced renal tubular senescence and fibrosis.

Automated summary

This study found that dihydroartemisinin can improve renal aging and injury by activating autophagy. It suggests that activation of autophagy and elimination of senescent cells may be an effective strategy for preventing kidney damage and fibrosis.