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Updated: Jun 27, 2025
Acute Kidney Injury Model Induced by Cisplatin in Adult Zebrafish
Published on: May 15, 2021
Protopanaxadiol prevents cisplatin-induced acute kidney injury by regulating ferroptosis
Zeyu Song1, Zhenyuan Li1, Tao Pan1
1School of Pharmacy, Key Laboratory of Molecular Pharmacology and Drug Evaluation (Yantai University), Ministry of Education, Collaborative Innovation Center of Advanced Drug Delivery System and Biotech Drugs in Universities of Shandong, Yantai University, Yantai 264005, PR China.
Objectives:
Acute kidney injury (AKI) caused by cisplatin (CDDP) is a complex, critical illness with no effective or specific treatment. The purpose of the study was to assess the protective effect of protopanaxadiol (PPD) on the kidneys in CDDP-induced AKI models and its possible mechanisms.
Methods:
In vitro, the protection of PPD was assessed in HK-2. KM mice were injected with CDDP to induce AKI models in vivo. The determination of blood urea nitrogen and serum creatinine (SCr) was performed, and pathological changes were examined by histopathological examination. Immunostaining and western blot analyses were used to analyze the expression levels of proteins.
Results:
PPD can increase the viability of HK-2 cells damaged by CDDP, improve cell morphology, and alleviate the symptoms of AKI in mice. In addition, PPD can down-regulate the protein expression of TRF and up-regulate the protein expression of Ferritin heavy chain, Glutathione peroxidase 4, and ferroptosis suppressor protein 1 reduce the iron content in cells and kidney tissues, and restore the antioxidant defense system.
Conclusion:
PPD has an inhibitory effect on cisplatin-induced nephrotoxicity, which may be related to the inhibition of ferroptosis by regulating iron metabolism and lipid peroxidation.
Insights
Protopanaxadiol (PPD) protects against cisplatin-induced acute kidney injury (AKI) by inhibiting ferroptosis. This study demonstrates PPD
Area of Science:
- Nephrology
- Pharmacology
- Biochemistry
Background:
- Cisplatin (CDDP) causes acute kidney injury (AKI), a critical condition lacking specific treatments.
- Understanding the mechanisms of CDDP-induced AKI is crucial for developing effective therapies.
Purpose of the Study:
- To evaluate the protective effects of protopanaxadiol (PPD) against CDDP-induced AKI.
- To elucidate the underlying mechanisms of PPD's protective action in kidney injury.
Main Methods:
- In vitro assessment of PPD in HK-2 cells exposed to CDDP.
- In vivo CDDP-induced AKI model in KM mice.
- Biochemical analysis (BUN, SCr) and histopathological examination.
- Immunostaining and Western blot for protein expression analysis.
Main Results:
- PPD enhanced HK-2 cell viability and improved kidney morphology in AKI models.
- PPD treatment down-regulated transferrin receptor (TRF) and up-regulated ferritin heavy chain, glutathione peroxidase 4, and ferroptosis suppressor protein 1.
- PPD reduced iron content and restored the antioxidant defense system in kidney tissues.
Conclusions:
- PPD exhibits significant protective effects against cisplatin-induced nephrotoxicity.
- PPD's mechanism involves the inhibition of ferroptosis via regulation of iron metabolism and lipid peroxidation.
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