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

Author:

Xue-Bai 1,Jie-Hu 1,Zhang Mei-Ling2,Juan-Luo 1,Liu Yu-Han1,Yue-Zhang 3,Hui-Kong 1,Qu Hui-Hua4,Yan-Zhao 1

Affiliation:

1. School of Traditional Chinese Medicine, Beijing University of Chinese Medicine, Beijing 100029, People’s Republic of China

2. Key Laboratory of Chinese Internal Medicine of the Ministry of Education, Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine, Beijing 100029, People’s Republic of China

3. School of Life Sciences, Beijing University of Chinese Medicine, Beijing 100029, People’s Republic of China

4. Centre of Scientific Experiment, Beijing University of Chinese Medicine, Beijing 100029, People’s Republic of China

Abstract

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-α (TNF-α), 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.

Publisher

American Scientific Publishers

Subject

Pharmaceutical Science,General Materials Science,Biomedical Engineering,Medicine (miscellaneous),Bioengineering

Reference92 articles.

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