期刊
MEDICINE
卷 97, 期 23, 页码 -出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MD.0000000000010920
关键词
angiogenesis; apoptosis; human fibroblast-like synovial cells; NF-kappa B pathway; proliferation; rheumatoid arthritis
资金
- National Natural Science Foundation of China [81402936, 81302576]
- Jiangsu Provincial Natural Science Foundation of China [BK20131234]
- Six Talent Peak Research Project in Jiangsu Province [2015-WSN-105]
- 333 Project of Jiangsu Province, Jiangsu Province Youth Medical Talent Project
- Jiangsu Province Clinical Medical Science and Technology Project [BL2013034]
Background: Rheumatoid arthritis (RA) is the most common inflammatory arthritis and is a major cause of disability. The nuclear factor-kappa-light-chain-enhancer of activated B cells (NF-kappa B) signaling pathway has been reported to be involved in the pathogenesis of RA with unclear mechanisms. Therefore, this study aims to explore the effect of NF-kappa B pathway on proliferation, apoptosis, and angiogenesis of human fibroblast-like synovial cells (HFLS) in RA. Methods: Normal HFLS and RA-HFLS were selected as the normal and control groups, respectively. RA-HFLS were treated by BAY11-7082 (an inhibitor of NF-kappa B) in different concentrations, namely 2.5 mu mol/L BAY11-7082, 5 mu mol/LBAY11-7082 and 10 mu mol/L BAY11-7082. MTT assay was employed to detect cell proliferation. Cell apoptosis was determined by flow cytometry at 24, 48, and 72hours after culture. Western blot analysis was employed to detect the expressions of NF-kappa B, angiogenesis-related factors (VEGF, Ang1, and Ang2). Results: Initially, we found that BAY11-7082 inhibited NF-kappa B expression in a concentration-dependent manner. According to the findings of MTT assay and flow cytometry, we understood that RA-HFLS treated by BAY11-7082 (an inhibitor of NF-kappa B), the inhibition of NF-kappa B pathway, suppressed RA-HFLS proliferation and induced RA-HFLS apoptosis in a concentration and time-(d) ependent manner. Furthermore, RA-HFLS treated by BAY11-7082 presented decreased VEGF, Ang1 and Ang2 expressions in a concentration-dependent manner. Conclusion: The study concluded that inhibition of NF-kappa B pathway induced cell apoptosis and suppressed proliferation and angiogenesis of RA-HFLS, which could serve as a novel target in the treatment of RA.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据