Silymarin/Silybin‐functionalized Selenium Nanoparticles Suppress Lipopolysaccharide‐induced Inflammation via PI3K/AKT/NF‐κB Signaling Pathway Inhibition
Ahmed Abdrabou, Khairy M. A. Zoheir, Ghada A. Abdel‐Aleem, Asmaa Osama B. S. Osman, Doaa T. Elsabagh, Mohamed S. Kishta
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.