Silymarin/Silybin‐functionalized Selenium Nanoparticles Suppress Lipopolysaccharide‐induced Inflammation via PI3K/AKT/NF‐κB Signaling Pathway Inhibition

Abstract

An immune system's natural defense mechanism in the face of dangerous stimuli including toxic chemicals is called inflammation. It is a good idea to regulate the production of the released cytokines upon anti-inflammatory and antioxidant applications. Silymarin (Sm), Silybin (Sb), and Selenium (Se) have anti-inflammatory and antioxidant activities. Formulation of these agents using nanotechnology will facilitate their entrance to cells and increase their efficacy. This study's primary objective is to assess the anti-inflammatory and antioxidant properties of Se nanoparticles (SeNPs), Sm-SeNPs, and Sb-SeNPs in vitro in bone marrow-derived mesenchymal stem cells (BM-MSCs) induced by lipopolysaccharides (LPS). The zeta potentials of SeNPs, Sm-SeNPs, and Sb-SeNPs were measured at -5.28, -35.3, and -30.5 mV, and their sizes were 78.82, 105.70, and 91.28 nm, respectively. Phosphoinositide 3-kinase (PI3K), protein kinase B (AKT), nuclear factor kappa B (NF-κB), and interleukin-1β mRNA expression levels and concentrations were significantly increased in the LPS-induced BM-MSCs. Tumor necrosis factor-α gene expression was upregulated upon LPS treatment. On the other hand, superoxide dismutase activity significantly decreased in the LPS-induced BM-MSCs, while catalase and glutathione peroxidase gene expressions were downregulated upon LPS treatment. Sm-SeNPs and Sb-SeNPs can overcome LPS-induced inflammatory and oxidative stress response in BM-MSCs through the inhibition of the PI3K/AKT/NF-κB signaling pathway.