Dynamic Compression in the Presence of TNF-Alpha Differentially Effects Gene Expression in Tibial Plateau Cartilage Covered and Uncovered by the Meniscus

Author(s):  
Scott L. Bevill ◽  
Thomas P. Andriacchi

It has been suggested that altered joint loading may be a cause of the cartilage degeneration commonly observed following joint destabilizing events such as anterior cruciate ligament (ACL) injury [1]. Changes in the biochemical environment of the joint accompany these changes in joint loading, though, with acute and chronic increases in synovial concentrations of proinflammatory cytokines such as tumor necrosis factor-alpha (TNFα) [2, 3]. TNFα is a potent catabolic factor associated with increased expression [4] and synthesis [5] of matrix proteases in articular cartilage, and therefore may play in important role in the degenerative events following joint injury.

Nutrients ◽  
2019 ◽  
Vol 11 (6) ◽  
pp. 1312 ◽  
Author(s):  
Yu-Wen Yen ◽  
Ying-Jiun Lai ◽  
Zwe-Ling Kong

Osteoarthritis (OA), also called degenerative joint disease, is characterized by joint cartilage loss and is strongly linked to obesity. Medicine to alleviate pain is currently the only treatment. Shiikuwasha extract (SE) has been reported to possess valuable bioactive substances exhibiting anti-inflammatory, antiobesity, and anticancer effects. Research is limited to the use of SE in the treatment of OA and obesity. We performed both anterior cruciate ligament transections and medial meniscectomies to induce OA on Sprague–Dawley rats after 11 weeks of a high fat diet followed by 9 weeks of oral SE administration (300, 600, and 1500 mg/kg). This study showed that SE treatment could reduce weight gain and joint pain. Additionally, SE significantly decreased triglycerides and total cholesterol in plasma of the S1500 group but increased high-density lipoprotein cholesterol in the plasma of the S600 group. Meanwhile, plasma levels of tumor necrosis factor alpha (TNF-α) was significantly reduced in the S1500 groups. Histopathological findings confirmed administration of SE attenuated cartilage degeneration. Immunohistochemistry examination demonstrated that caspase 3 and phospho-Janus kinase 2 (p-JAK2) expression levels on chondrocytes were downregulated by SE treatment. Our findings demonstrate that SE can alleviate OA progression by improving obesity.


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