4.5 Article

Protective Effect of Nanoparticles from Platycladi Cacumen Carbonisata on 2,4,6-Trinitrobenzene Sulfonic Acid (TNBS)-Induced Colitis in Rats

Journal

JOURNAL OF BIOMEDICAL NANOTECHNOLOGY
Volume 18, Issue 2, Pages 422-434

Publisher

AMER SCIENTIFIC PUBLISHERS
DOI: 10.1166/jbn.2022.3248

Keywords

Nanoparticles; Platycladi Cacumen Carbonisata; TNBS-Induced Colitis; Anti-Inflammation; Antioxidative Stress

Funding

  1. Special Funds for Fundamental Research Expenses of Central Universities [2019-JYB-TD-001]

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This study evaluates the protective effects of Platycladi Cacumen Carbonisata-derived nanoparticles against ulcerative colitis in rats. The nanoparticles showed potential therapeutic effects by regulating inflammatory factors and improving resistance to oxidative stress.
Aim: To evaluate the protective effects of Platycladi Cacumen Carbonisata-derived nanoparticles (PCC-NPs) against 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced ulcerative colitis (UC) in rats. Methods: This study developed and characterized novel PCC-NPs synthesized by a green and simple pyrolysis process using Platycladi Cacumen (PC) as the sole precursor. The UC model prepared with rectal instillation of TNBS was used to evaluate the potential efficacy of PCC-NPs, and the underlying mechanisms were preliminarily explored from the perspective of anti-inflammatory and antioxidative stress for the first time. Results: PCC-NPs exhibited low cytotoxicity, good dispersibility and copious surface functional groups. Nanoparticles with diameters ranging from 40-60 nm mainly manifested a therapeutic effect by downregulating tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and upregulating interleukin-10 (IL-10). In addition, PCC-NPs relieved colon injury by inhibiting myeloperoxidase (MPO) activity, limiting the release of malondialdehyde (MDA) and increasing the activity of superoxide dismutase (SOD). Conclusion: Green synthetic PCC-NPs is a potential candidate as a complementary drug for intestinal inflammation of inflammatory bowel disease, and its regulatory mechanisms may be to balance the levels of pro-/anti-inflammatory cytokines and improve resistance to oxidative stress.

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