Anti-inflammatory and anti-catabolic effects of TENDOACTIVE® on human tenocytes in vitro.

污渍 炎症 化学 基质金属蛋白酶 细胞生物学 细胞外基质 αBκ 细胞凋亡 NF-κB 免疫学 生物 生物化学 基因
作者
Mehdi Shakibaei,Constanze Buhrmann,Ali Mobasheri
出处
期刊:PubMed [National Institutes of Health]
卷期号:26 (9): 1173-85 被引量:26
标识
DOI:10.14670/hh-26.1173
摘要

Tendons have a limited capacity for self-repair due to the low density and mitotic activity of tenocytes. Pro-inflammatory cytokines such as interleukin-1β (IL-1β) have been identified as the main initiators of tendinopathies, stimulating inflammation, apoptosis and extracellular matrix (ECM) degradation. The aim of this study was to evaluate the potential of Tendoactive®, a newly developed proprietary nutraceutical formulation that includes mucopolysaccharides, collagen and vitamin C, in an in vitro model of tendon inflammation. The effects of Tendoactive® were studied in primary cultures of human tenocytes treated with IL-1β for up to 72 h. Expression of collagen type I, integrin β1, cyclo-oxygenase-2 (COX-2), caspase-3 and matrix metalloproteinase-1 (MMP-1) was monitored by western blotting. The effects of Tendoactive® on the expression, phosphorylation and nuclear translocation of protein components of the NF-κB system were studied by western blotting and immunofluorescence respectively. Treatment of tenocytes with Tendoactive® suppressed IL-1β-induced NF-κB activation and p65 nuclear translocation. These events correlated with down-regulation of NF-κB targets including COX-2, MMP-1 and activated caspase-3. Tendoactive® also reversed the IL-1β-induced down-regulation of collagen type I and β1-integrin receptor expression. These results indicate that Tendoactive® has nutraceutical potential as an anti-inflammatory agent for treating tendinopathy through suppression of NF-κB mediated IL-1β catabolic signalling pathways in tenocytes.

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