Grown on Germinated (GRC) Encapsulated in Chitosan Nanoparticle (GCN) Suppresses Particulate Matter (PM)-Induced Lung Inflammation in Mice.

Int J Mol Sci

Department of Food Science and Biotechnology, College of BioNano Technology, Gachon University, Seongnam-si 13120, Republic of Korea.

Published: October 2024

AI Article Synopsis

  • GRC (germinated rice) shows anti-inflammatory, anti-allergic, and immune-regulatory effects, and this study focuses on its anti-inflammatory properties when encapsulated in chitosan nanoparticles (CN) against lung inflammation caused by particulate matter (PM).
  • The optimized chitosan nanoparticles (referred to as CN6) demonstrated suitable characteristics for encapsulation, particularly with a specific GRC concentration (8 mg/mL) leading to effective entrapment and loading efficiency.
  • In vivo studies on mice showed significant reductions in immune cell infiltration and lung damage from PM when treated with GRC encapsulated in CN, alongside promising results in cell culture models that indicated potential for managing PM-related inflammatory lung disease.

Article Abstract

grown on germinated (GRC) exerts various biological effects, including anti-allergic, anti-inflammatory, and immune-regulatory effects. In this study, we investigated the anti-inflammatory effects of GRC encapsulated in chitosan nanoparticles (CN) against particulate matter (PM)-induced lung inflammation. Optimal CN (CN6) (CHI: TPP ratio of 4:1; TPP pH 2) exhibited a zeta potential of +22.77 mV, suitable for GRC encapsulation. At different GRC concentrations, higher levels (60 and 120 mg/mL) led to increased negative zeta potential, enhancing stability. The optimal GRC concentration for maximum entrapment (31.4 ± 1.35%) and loading efficiency (7.6 ± 0.33%) of GRC encapsulated in CN (GCN) was 8 mg/mL with a diameter of 146.1 ± 54 nm and zeta potential of +30.68. In vivo studies revealed that administering 300 mg/kg of GCN significantly decreased the infiltration of macrophages and T cells in the lung tissues of PM-treated mice, as shown by immunohistochemical analysis of CD4 and F4/80 markers. Additionally, GCN ameliorated PM-induced lung tissue damage, inflammatory cell infiltration, and alveolar septal hypertrophy. GCN also decreased total cells and neutrophils, showing notable anti-inflammatory effects in the bronchoalveolar lavage fluid (BALF) from PM-exposed mice, compared to GRC. Next the anti-inflammatory properties of GCN were further explored in PM- and LPS-exposed RAW264.7 cells; it significantly reduced PM- and LPS-induced cell death, NO production, and levels of inflammatory cytokine mRNAs (IL-1β, IL-6, and COX-2). GCN also suppressed NF-κB/MAPK signaling pathways by reducing levels of p-NF-κB, p-ERK, and p-c-Jun proteins, indicating its potential in managing PM-related inflammatory lung disease. Furthermore, GCN significantly reduced PM- and LPS-induced ROS production. The enhanced bioavailability of GRC components was demonstrated by an increase in fluorescence intensity in the intestinal absorption study using FITC-GCN. Our data indicated that GCN exhibited enhanced bioavailability and potent anti-inflammatory and antioxidant effects in cells and in vivo, making it a promising candidate for mitigating PM-induced lung inflammation and oxidative stress.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11477187PMC
http://dx.doi.org/10.3390/ijms251910642DOI Listing

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