Literature Express | Qihengxing reverse transcription and dye-based qPCR products facilitate cancer research

Nephrotoxicity is a common side effect in cancer patients receiving chemotherapy. The pathogenesis of chemotherapy-induced nephrotoxicity involves multiple factors such as oxidative stress, DNA damage, inflammation, and apoptosis. Omega-3 polyunsaturated fatty acids (ω-3 PUFAs), especially 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, which explored the effects of EPA and DHA alone or in combination on cisplatin-induced nephrotoxicity in mice and their potential mechanisms (Figure 1).

Qihengxing reverse transcription and dye-based qPCR reagents facilitate this research!

Cisplatin is a widely used chemotherapy drug, but it can cause renal toxicity including oxidative stress, DNA damage, inflammation, and apoptosis. Omega-3 PUFAs have anti-inflammatory and antioxidant properties, can protect the cardiovascular and nervous systems, reduce the risk of diabetes, and relieve depressive symptoms. Omega-3 PUFAs can 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 conducted experiments at the cellular level using the HK-2 cell line to evaluate the effects of EPA and DHA on cisplatin-induced cytotoxicity. The results showed that ω-3 PUFAs can alleviate cisplatin-induced kidney damage, reduce oxidative stress and inflammation, and inhibit cell apoptosis. The combined use of EPA and DHA is more effective than using them alone, especially in inhibiting weight loss and reducing serum creatinine, blood urea nitrogen (BUN), and neutrophil gelatinase-associated lipoprotein (NGAL) levels.

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

In conclusion, this study shows that the intake of ω-3 PUFAs may be used as a therapeutic strategy to prevent and treat cisplatin-induced nephrotoxicity. This study provides a scientific basis for the use of ω-3 PUFAs in the prevention and treatment of cisplatin-related nephrotoxicity in the clinic, which may help improve the treatment outcomes and quality of life of cancer patients. It also demonstrates the potential therapeutic value of ω-3 PUFAs in alleviating cisplatin-induced nephrotoxicity and reveals the molecular mechanism behind it.