The Protective Effect of Selenium Nanoparticles in Osteoarthritis: In vitro and in vivo Studies

被引:5
|
作者
Li, Yong [1 ,2 ]
Zhu, Senbo [2 ]
Luo, Junchao [2 ]
Tong, Yu [2 ]
Zheng, Yixuan [1 ]
Ji, Lichen [2 ]
He, Zeju [2 ]
Jing, Qiangan [1 ]
Huang, Jiaqing [2 ]
Zhang, Yinjun [1 ]
Bi, Qing [2 ]
机构
[1] Zhejiang Univ Technol, Coll Biotechnol & Bioengn, Hangzhou 310014, Zhejiang, Peoples R China
[2] Zhejiang Prov Peoples Hosp, Affiliated Peoples Hosp, Hangzhou Med Coll, Dept Lab Med,Lab Med Ctr, Hangzhou 310014, Zhejiang, Peoples R China
来源
基金
美国国家科学基金会;
关键词
osteoarthritis; NF-kappa B p65 signaling pathway; p38/MAPK signaling pathway; selenium nanoparticles; NF-KAPPA-B; INFLAMMATORY MEDIATORS; MATRIX METALLOPROTEINASES; INDUCED EXPRESSION; OXIDATIVE STRESS; MMP EXPRESSION; CHONDROCYTES; P38; ACTIVATION; INHIBITION;
D O I
10.2147/DDDT.S407122
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Introduction: Osteoarthritis (OA) is a common chronic joint disease characterized by articular cartilage degeneration. OA usually manifests as joint pain, limited mobility, and joint effusion. Currently, the primary OA treatment is non-steroidal anti-inflammatory drugs (NSAIDs). Although they can alleviate the disease's clinical symptoms and signs, the drugs have some side effects. Selenium nanoparticles (SeNPs) may be an alternative to relieve OA symptoms. Materials and Results: We confirmed the anti-inflammatory effect of selenium nanoparticles (SeNPs) in vitro and in vivo experiments for OA disease in this study. In vitro experiments, we found that SeNPs could significantly reduce the expression of nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), the major inflammatory factors, and had significant anti-inflammatory and anti-arthritic effects. SeNPs can inhibit reactive oxygen species (ROS) production and increased glutathione peroxidase (GPx) activity in interleukin-1beta (IL-1 ss)-stimulated cells. Additionally, SeNPs down-regulated matrix metalloproteinase-13 (MMP-13) and thrombospondin motifs 5 (ADAMTS-5) expressions, while up-regulated type II collagen (COL-2) and aggrecan (ACAN) expressions stimulated by IL-1 ss. The findings also indicated that SeNPs may exert their effects through suppressing the NF-.B p65 and p38/MAPK pathways. In vivo experiments, the prevention of OA development brought on by SeNPs was demonstrated using a DMM model. Discussion: Our results suggest that SeNPs may be a potential anti-inflammatory agent for treating OA.
引用
收藏
页码:1515 / 1529
页数:15
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