ArticleBiological trace element research2026
Oridonin Protects Mice Against Cadmium-induced Kidney Injury by Inhibiting Ferroptosis via SIRT1 Regulation.
Article in Biological trace element research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Kidney injury is a clinical condition characterized by a rapid decline in renal function, associated with high morbidity and mortality. This study aimed to investigate the protective effects and mechanism of oridonin against cadmium-induced kidney injury in mice. A mouse model of cadmium-induced kidney injury was established by cadmium administration. Inflammatory cytokines were tested by ELISA. Protein expression was measured by western blot analysis. Oridonin treatment reduced cadmium-induced serum creatinine and blood urea nitrogen (BUN), kidney myeloperoxidase (MPO) activity, and TNF-α and IL-1β production. Oridonin also alleviated pathological changes in the kidney caused by cadmium. Furthermore, cadmium-induced hypoxia-inducible factor-1α (HIF-1α), NLRP3 inflammasome and NF-κB activation were inhibited by oridonin. Oridonin also suppressed cadmium-induced ferroptosis. In addition, oridonin upregulated SIRT1 expression and the protective effects of oridonin on cadmium-induced inflammation and ferroptosis were abolished by SIRT1 inhibitor. In conclusion, oridonin attenuates cadmium-induced kidney injury by activating SIRT1, which in turn suppresses inflammation and ferroptosis.
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