In clinical practice, cisplatin is the most commonly used chemotherapy drug to treat a range of malignancies. Severe ROS-regulated nephrotoxicity, however, restricts its applicability. Currently, the main mechanisms leading to cisplatin-induced nephrotoxicity in clinical settings involve hydration or diuresis. However, not all patients can be treated with massive hydration or diuretics. Therefore, it is crucial to develop a treatment modality that can effectively reduce nephrotoxicity through a foodborne route. Selenium has been reported to have strong antioxidant as well as anticancer effects when administered as spore oil. Herein, we established cellular and animal models of cisplatin-induced nephrotoxicity and synthesized spore oil-functionalized nano-selenium (GLSO@SeNPs). We found that GLSO@SeNPs inhibit the mitochondrial apoptotic pathway by maintaining oxidative homeostasis and regulating related signaling pathways (the MAPK, caspase, and AKT signaling pathways). In vivo, GLSO@SeNPs could effectively improve cisplatin-induced renal impairment, effectively maintaining oxidative homeostasis in renal tissues and thus inhibiting the process of renal injury. In addition, GLSO@SeNPs were converted into selenocysteine (SeCys2), which may exert protective effects. Furthermore, GLSO@SeNPs could effectively modulate the ratio of immune cells in kidneys and spleen, reducing the proportions of CD3+CD4+ T cells, CD3+CD8+ T cells, and M1 phenotype macrophages and increasing the proportion of anti-inflammatory regulatory T cells. In summary, in this study, we synthesized food-derived spore oil-functionalized nanomaterials, and we explored the mechanisms by which GLSO@SeNPs inhibit cisplatin-induced nephrotoxicity. Our study provides a basis and rationale for the inhibition of cisplatin-induced nephrotoxicity by food-derived nutrients.

Platinum-based metal complexes especially cisplatin (cis-diamminedichloroplatinum II, CDDP) possesses strong anticancer properties and a broad anticancer spectrum. However, the clinical application of CDDP has been limited by its side effects...

Oxidative stress damage of pancreatic β-cells is a key link in the pathogenesis of type 2 diabetes mellitus. A long-term increase of free fatty acids induces the increase of reactive oxygen species (ROS) in β-cells, leading to apoptosis and dysfunction of β-cells. Ganoderma lucidum spore oil (GLSO) is a functional food complex with strong antioxidant activity, but its solubility and stability are poor. In the present study, GLSO-functionalized selenium nanoparticles (GLSO@SeNPs) with high stability and uniform particle size were synthesized by a high-pressure homogeneous emulsification method. The aim of this study was to investigate the protective effects of GLSO@SeNPs on INS-1E rat insulinoma β-cells against palmitic-acid (PA)-induced cell death, as well as the underlying mechanisms. Our results showed that GLSO@SeNPs had good stability and biocompatibility, and they significantly inhibited the PA-induced apoptosis of INS-1E pancreatic cells by regulating the activity of related antioxidant enzymes, including thioredoxin reductase (TrxR), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px). Western blot analysis showed that GLSO@SeNPs reversed the PA-induced changes in MAPK pathway protein expression levels. Thus, the present findings provided a new theoretical basis for utilizing GLSO@SeNPs as a treatment for type 2 diabetes.