The kidney is a high-energy demand organ rich in mitochondria especially renal tubular cells. Emerging evidence suggests that
mitochondrial dysfunction, redox imbalance and kidney injury are interconnected.
Artemether has biological effects by targeting mitochondria and exhibits potential therapeutic value for
kidney disease. However, the underlying molecular mechanisms have not been fully elucidated. This study was performed to determine the effects of
artemether on
Adriamycin-induced nephropathy and the potential mechanisms were also investigated. In vivo, an
Adriamycin nephropathy mouse model was established, and mice were treated with or without
artemether for 2 weeks. In vitro, NRK-52E cells were stimulated with TGF-β1 and treated with or without
artemether for 24 h. Then renal damage and cell changes were evaluated. The results demonstrated that
artemether reduced urinary
protein excretion, recovered podocyte alterations, attenuated pathological changes and alleviated renal tubular injury.
Artemether also downregulated TGF-β1
mRNA expression levels, inhibited tubular proliferation, restored tubular cell phenotypes and suppressed proliferation-related signalling pathways. In addition,
artemether restored renal redox imbalance, increased
mtDNA copy number and improved mitochondrial function. In summary, we provided initial evidence that
artemether ameliorates kidney injury by restoring redox imbalance and improving mitochondrial function in
Adriamycin nephropathy in mice.
Artemether may be a promising agent for the treatment
kidney disease.