Evidence map›Paper›PMID 42503588›Full record

ArticleBiological trace element research2026

Oridonin Protects Mice Against Cadmium-induced Kidney Injury by Inhibiting Ferroptosis via SIRT1 Regulation.

Sixuan Li, Siqi Liu, Huafeng Geng, Yang Li, Cong Ye, Chunxi Wang, Yue Zhang

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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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1 · What the graph read from it

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Sixuan LiCollege of Animal Science and Technology, Jilin Agriculture Science and Technology University, Jilin City, China.
Siqi LiuDepartment of Urology, The First Hospital of Jilin University, 1 Xinmin Street, Changchun, 130061, China.
Huafeng GengDepartment of Gynecology, China-Japan Union Hospital of Jilin University, Changchun, 130033, Jilin, China.
Yang LiDepartment of Gynecology, China-Japan Union Hospital of Jilin University, Changchun, 130033, Jilin, China.
Cong YeDepartment of Gynecology, China-Japan Union Hospital of Jilin University, Changchun, 130033, Jilin, China.
Chunxi WangDepartment of Urology, The First Hospital of Jilin University, 1 Xinmin Street, Changchun, 130061, China.
Yue ZhangCollege of Animal Science and Technology, Jilin Agriculture Science and Technology University, Jilin City, China. zhangyue888@jlnku.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Acute Kidney InjuryCadmiumDiterpenes, KauraneFerroptosisSirtuin 1AnimalsKidneyMaleMiceCadmiumDiterpenes, KauraneoridoninSirt1 protein, mouseSirtuin 1CadmiumFerroptosisKidney injuryMPONLRP3

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.