# Poria cocos Polysaccharide-Modified Selenium Nanoparticles: Structural Characterization, Stability, and In Vitro Antioxidant and Anti-Inflammatory Activity Studies

**Authors:** Tao Shu, Fan Li, Jiang-Ning Hu, Yu Xu

PMC · DOI: 10.3390/foods14203555 · 2025-10-18

## TL;DR

Researchers developed stable selenium nanoparticles modified with a polysaccharide from Poria cocos, which showed antioxidant and anti-inflammatory effects in cell studies.

## Contribution

The novel use of Poria cocos polysaccharide to modify Se NPs improves stability and biological activity.

## Key findings

- PCP-Se NPs showed excellent stability in storage and salt ion environments.
- PCP-Se NPs effectively scavenged free radicals and reduced inflammation in RAW264.7 cells.
- The nanoparticles maintained mitochondrial function and reduced oxidative stress markers.

## Abstract

Selenium nanoparticles (Se NPs) have received increasing attention as a new alternative source to other forms of selenium in nutritional dietary supplements; however, the limited stability and pronounced tendency of selenium nanoparticles (Se NPs) to aggregate in aqueous environments have significantly constrained their practical applications. In this study, Poria cocos polysaccharide-modified Se NPs (PCP-Se NPs) were synthesized by the selenite/ascorbic acid chemical reduction method. PCP-Se NPs exhibited a uniformly dispersed spherical morphology with an average particle size of 66.64 ± 0.30 nm, and displayed an amorphous crystal structure. Compared to unmodified Se NPs, the PCP-Se NPs exhibited low Se release (8.83 ± 0.73%) after simulated gastrointestinal digestion, and they had excellent storage stability and salt ion stability. PCP-Se NPs exhibited potent antioxidant activity manifested by the effective scavenging of DDPH and ABTS radicals. PCP-Se NPs were efficiently internalized by RAW264.7 cells and released into the cytoplasm by a lysosomal escape mechanism, thereby effectively reducing intracellular inflammatory factor levels (the levels of MPO, NO, iNOS, TNF-α, IL-1β, and IL-10 in the PCP-Se NPs treatment group were 0.38 ± 0.013-fold, 0.26 ± 0.02-fold, 0.36 ± 0.02-fold, 0.57 ± 0.03-fold, 0.35 ± 0.02-fold, and 2.07 ± 0.16-fold that of the LPS group, respectively), alleviating oxidative stress (the levels of CAT, SOD, GSH, and MDA in the PCP-Se NP-treated group were 2.48 ± 0.02-fold, 1.91 ± 0.11-fold, 3.16 ± 0.28-fold, and 0.46 ± 0.03-fold that of the LPS group, respectively), and maintaining mitochondrial membrane potential stability. This study provides a basis and reference for improving the stability of Se NPs and developing novel selenium-enriched dietary supplements.

## Linked entities

- **Proteins:** MPO (myeloperoxidase), Nos1 (nitric oxide synthase 1, neuronal), NOS2 (nitric oxide synthase 2), TNF (tumor necrosis factor), IL1B (interleukin 1 beta), IL10 (interleukin 10), CAT (catalase), SOD1 (superoxide dismutase 1), LOC23687505 (pyrimidodiazepine synthase), so (sine oculis)
- **Chemicals:** selenium (PubChem CID 6326970), selenite (PubChem CID 1090), ascorbic acid (PubChem CID 9888239), DDPH (PubChem CID 163906), ABTS (PubChem CID 35688)

## Full-text entities

- **Genes:** Cat (catalase) [NCBI Gene 12359] {aka 2210418N07, Cas-1, Cas1, Cs-1}, Mpo (myeloperoxidase) [NCBI Gene 17523] {aka mKIAA4033}, Il1b (interleukin 1 beta) [NCBI Gene 16176] {aka IL-1beta, Il-1b}, Il10 (interleukin 10) [NCBI Gene 16153] {aka CSIF, If2a, Il-10}, Tnf (tumor necrosis factor) [NCBI Gene 21926] {aka DIF, TNF-a, TNF-alpha, TNFSF2, TNFalpha, Tnfa}, Nos2 (nitric oxide synthase 2, inducible) [NCBI Gene 18126] {aka MAC-NOS, NOS-II, Nos-2, Nos2a, i-NOS, iNOS}
- **Diseases:** Inflammatory (MESH:D007249)
- **Chemicals:** LPS (MESH:D008070), ascorbic acid (MESH:D001205), NO (MESH:D009614), selenite (MESH:D020887), Se (MESH:D012643), salt (MESH:D012492), MDA (MESH:D015104), PCP (-), ABTS (MESH:C002502), DDPH (MESH:C057485)
- **Cell lines:** RAW264.7 — Mus musculus (Mouse), Mouse leukemia, Cancer cell line (CVCL_0493)

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12563372/full.md

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Source: https://tomesphere.com/paper/PMC12563372