Silymarin-Functionalized Selenium Nanoparticles Prevent LPS- Induced Inflammatory Response in RAW264.7 Cells through Downregulation of the PI3K/Akt/NF-Kappa B Pathwayopen access
- Authors
- Mi, Xiao-jie; Le, Ha-Minh; Lee, Sanghyun; Park, Hye-Ryung; Kim, Yeon-Ju
- Issue Date
- Nov-2022
- Publisher
- AMER CHEMICAL SOC
- Citation
- ACS OMEGA, v.7, no.47, pp 42723 - 42732
- Pages
- 10
- Journal Title
- ACS OMEGA
- Volume
- 7
- Number
- 47
- Start Page
- 42723
- End Page
- 42732
- URI
- https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/68290
- DOI
- 10.1021/acsomega.2c04140
- ISSN
- 2470-1343
- Abstract
- Silymarin exhibits an anti-inflammatory property in various cancers and inflammatory diseases. In our previous work, silymarin-mediated selenium nanoparticles (SeNPs) (Si-SeNPs) were developed using a green synthesis technique, and its potential as an anticancer agent was confirmed. In order to further examine the extended comprehensive potential of Si-SeNPs, this investigation focuses on studying the enhanced anti-inflammatory effect of Si-SeNPs in lipopolysaccharide (LPS)-stimulated RAW264.7 macro-phages. Enzyme-linked immunosorbent assay and quantitative reverse transcription-polymerase chain reaction were used to evaluate the expression of pro-inflammatory mediators and cytokines. Western blotting and immunofluorescence assays were conducted to assess the protein expression of p-PI3K, p-Akt, p-NF-kappa B, and p-I kappa B alpha. Compared to silymarin, Si-SeNPs exhibited a significantly increased inhibitory effect on LPS-induced release of nitric oxide and the expression of pro-inflammatory cytokines such as tumor necrosis factor-alpha (TNF-alpha) and interleukin 1 beta (IL-1 beta) in RAW264.7 cells. A western blot assay indicated that Si-SeNPs downregulated the PI3K/Akt and NF-kappa B signaling pathways. The immunofluorescence assay suggested that Si-SeNPs inhibited the nuclear translocation and the activation of NF-kappa B. In addition, 740 Y-P (PI3K agonist) was used to demonstrate that activating the PI3K/Akt signal could partially reverse the inflammatory response, suggesting a causal role of the PI3K/Akt signaling pathway in the anti-inflammatory effect of Si-SeNPs. Consequently, these findings indicate that Si-SeNPs could be a functional agent of the attenuation of LPS-induced inflammatory responses in RAW264.7 macrophages through inhibiting the PI3K/Akt/NF-kappa B signaling pathway. In addition, biosynthesized Si-SeNPs could be more effective at reducing inflammation than only silymarin extracts. Thus, this study lays an experimental foundation for the clinical application of using biosynthesized SeNPs as a novel candidate in the field of inflammation-associated diseases.
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