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Nephrotoxicity is a common side effect in cancer patients receiving chemotherapy. The pathogenesis of chemotherapy-induced nephrotoxicity involves multiple factors, including oxidative stress, DNA damage, inflammation, and apoptosis. Omega-3 polyunsaturated fatty acids (ω-3 PUFAs), particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), have anti-inflammatory and antioxidant properties.

Teacher Mu Yunping from Guangdong University of Technology Recently "International Journal of Biological Macromolecules" (IF7.7) The article "Omega-3 polyunsaturated fatty acids protect against cisplatin-induced nephrotoxicity by activating the Nrf2 signaling pathway" was published, exploring the effects of EPA and DHA alone or in combination on cisplatin-induced nephrotoxicity in mice and the underlying mechanisms (Figure 1).

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Cisplatin, a widely used chemotherapy drug, can cause nephrotoxicity, including oxidative stress, DNA damage, inflammation, and apoptosis. Omega-3 PUFAs have anti-inflammatory and antioxidant properties that can protect the cardiovascular and nervous systems, reduce the risk of diabetes, and alleviate depressive symptoms. Omega-3 PUFAs also reduce the risk of complications in cancer patients and are associated with a reduced risk of chronic kidney disease (CKD).

Figure 1. Schematic diagram of the renal protective effects of ω-3 PUFAs through activation of the Nrf2 antioxidant and anti-apoptotic signaling pathways.

The researchers first evaluated the effects of EPA and DHA on cisplatin-induced cytotoxicity at the cellular level using the HK-2 cell line. The results demonstrated that ω-3 PUFAs mitigated cisplatin-induced renal damage, reduced oxidative stress and inflammation, and inhibited cell apoptosis. The combined use of EPA and DHA was more effective than either alone, particularly in inhibiting weight loss and reducing serum creatinine, blood urea nitrogen (BUN), and neutrophil gelatinase-associated lipoprotein (NGAL) levels.

Secondly, in animal models, cisplatin-induced acute kidney injury (AKI) and chronic kidney disease (CKD) were established in C57BL/6J mice to evaluate the protective effects of EPA and DHA. ω-3 PUFAs can induce p62 accumulation, downregulate Keap1 levels, and promote Nrf2 activation. ω-3 PUFAs enhance antioxidant gene expression by activating the p62-Keap1-Nrf2 signaling pathway and inhibit cisplatin-induced p53 apoptosis signaling through the Nrf2-MDM2 pathway.

In conclusion, this study suggests that ω-3 PUFA intake may serve as a therapeutic strategy for preventing and treating cisplatin-induced nephrotoxicity. This study provides scientific evidence for the clinical use of ω-3 PUFAs in preventing and treating cisplatin-related nephrotoxicity, potentially improving treatment outcomes and quality of life for cancer patients. It also demonstrates the potential therapeutic value of ω-3 PUFAs in alleviating cisplatin-induced nephrotoxicity and reveals the underlying molecular mechanisms.