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Updated: Apr 29, 2026
Acute Kidney Injury Model Induced by Cisplatin in Adult Zebrafish
Published on: May 15, 2021
The pseudoginsenoside F11 ameliorates cisplatin-induced nephrotoxicity without compromising its anti-tumor activity
Hongbo Wang1, Liang Kong1, Jianqiao Zhang2
11] Key Laboratory of Molecular Pharmacology and Drug Evaluation (Ministry of Education of China), School of Pharmacy, Yantai University, Yantai 264005, China [2].
Abstract:
The clinical use of cisplatin was severely limited by its associated nephrotoxicity. In this study, we investigated whether the pseudoginsenoside F11 had protective effects against cisplatin-induced nephrotoxicity. To clarify it, one in vivo model of cisplatin-induced acute renal failure was performed. The results showed that pretreatment with F11 reduced cisplatin-elevated blood urea nitrogen and creatinine levels, as well as ameliorated the histophathological damage. Further studies showed that F11 could suppress P53 activation, inverse the ratio of Bax/Bcl2 and the anti-oxidative and free radical levels induced by cisplatin, which in turn inhibited tubular cell apoptosis. Importantly, F11 enhanced rather than inhibited the anti-tumor activity of cispaltin in murine melanoma and Lewis lung cancer xenograft tumor models. Our findings suggested that administering F11 with cisplatin might alleviate the associated nephrotoxicity without compromising its therapeutic efficiency. This finding provides a novel potential strategy in the clinical treatment of cancer.
Insights
Pseudoginsenoside F11 protects against cisplatin-induced kidney damage by reducing apoptosis and oxidative stress. This compound also enhances cisplatin's anti-tumor effects, offering a novel cancer treatment strategy.
Area of Science:
- Pharmacology
- Nephrology
- Oncology
Background:
- Cisplatin is a vital chemotherapy drug, but its clinical application is limited by severe nephrotoxicity.
- Developing strategies to mitigate cisplatin-induced kidney damage is crucial for improving cancer patient outcomes.
Purpose of the Study:
- To investigate the protective effects of pseudoginseng F11 against cisplatin-induced nephrotoxicity.
- To evaluate whether pseudoginseng F11 affects the anti-tumor efficacy of cisplatin.
Main Methods:
- An in vivo model of cisplatin-induced acute renal failure was employed.
- Histopathological damage, blood urea nitrogen, and creatinine levels were assessed.
- P53 activation, Bax/Bcl2 ratio, and oxidative stress markers were analyzed.
- Anti-tumor activity was evaluated in murine melanoma and Lewis lung cancer xenograft models.
Main Results:
- Pseudoginseng F11 pretreatment significantly reduced cisplatin-induced elevations in blood urea nitrogen and creatinine.
- F11 ameliorated kidney histopathological damage and inhibited tubular cell apoptosis.
- F11 suppressed P53 activation, modulated the Bax/Bcl2 ratio, and reduced oxidative stress.
- F11 enhanced, rather than inhibited, the anti-tumor activity of cisplatin in vivo.
Conclusions:
- Pseudoginseng F11 demonstrates significant nephroprotective effects against cisplatin-induced kidney injury.
- F11 alleviates nephrotoxicity without compromising cisplatin's anti-cancer efficacy.
- Combining F11 with cisplatin presents a promising strategy for cancer therapy, improving safety and effectiveness.
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