Effect of Meridian-Sinew Release Therapy on Moderate Knee Osteoarthritis in Patients, and on the TLR4/MYD88/NF-κB Signaling Transduction Pathway In Vitro

被引:3
|
作者
Wang, Chen [1 ,2 ]
Wei, Song [1 ]
Li, Xiaohao [1 ]
Chen, Zhihuang [1 ]
Hou, Chunfu [1 ]
Li, Hui [1 ]
Guo, Jing [1 ]
Wang, Shuting [1 ]
机构
[1] Chinese PLA, Guangzhou Mil Area Command, Guangzhou Gen Hosp, Dept Tradit Chinese Med, Guangzhou 510010, Guangdong, Peoples R China
[2] Guangzhou Univ Tradit Chinese Med, Guangzhou 510403, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
Knee Osteoarthritis; Meridian-Sinew Release Therapy; Synovial; TLR4/NF-kappa B; Inflammatory Factors; TOLL-LIKE RECEPTORS; MATRIX METALLOPROTEINASES; TOLL-LIKE-RECEPTOR-4; PATHOGENESIS; EXPRESSION; ARTHRITIS; DISEASES; PROTEIN;
D O I
10.1166/nnl.2018.2791
中图分类号
TB3 [工程材料学];
学科分类号
0805 ; 080502 ;
摘要
Knee osteoarthritis (KOA) is a degenerative joint disease that is very common amongst the elderly. There is currently no effective treatment to manage existing KOA or to delay its progression. Meridian-sinew release therapy (MSRT) is a new treatment based on the channel tendon theory. We evaluated the clinical effects of MSRT in patients with KOA, with favorable results indicating long-term benefits with few adverse effects. We used qRT-PCR, western blot analysis and immunohistochemical analysis to investigate the expression of genes related to synovial tissue inflammation in patients with KOA before and after MSRT. The findings confirmed that MSRT decreased expression of inflammatory factors including Interleukin-1 alpha (IL-1 beta), Interleukin-6 (IL-6), Interleukin-8 (IL-8), Tumour necrosis factor-alpha (TNF-alpha) and Matrix metallopeptidase-13 (MMP-13). This was achieved by down-regulation of the TLR4/MyD88/NF-kappa B signal transduction pathway, and resulted in alleviation of the clinical symptoms of KOA. Elucidation of the molecular mechanism underpinning MSRT in patients with KOA sheds light that facilitates future wider application of MSRT in KOA and other inflammatory diseases.
引用
收藏
页码:1433 / 1440
页数:8
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