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首页> 外文期刊>Osteoarthritis and cartilage >SIRT1, a class III histone deacetylase, regulates TNF-??-induced inflammation in human chondrocytes
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SIRT1, a class III histone deacetylase, regulates TNF-??-induced inflammation in human chondrocytes

机译：SIRT1，III类组蛋白脱乙酰基酶，调节TNF-α诱导的人软骨细胞炎症

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Objective: The present study was performed to elucidate the possible role of SIRT1 signaling in joint inflammation in human articular chondrocytes. Design: Real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) and Western blotting were performed to detect gene products and proteins involved in tumor necrosis factor ?? (TNF-??)-induced inflammation and cartilage degradation in human primary chondrocytes. Matrix metalloproteinase (MMP)-2 and MMP-9 activity was evaluated by gelatin zymography. Overexpression and knockdown of SIRT1 were also performed to investigate whether SIRT1 is associated with the anti-inflammatory activity of resveratrol in chondrocytes. Results: Resveratrol dose-dependently inhibited TNF-??-induced cyclooxygenase-2 (COX-2), MMP-1, MMP-3, MMP-13 and PGE2 production in human chondrocytes. Moreover, MMP-2 and MMP-9 activity was increased by treatment with TNF-??; however, SIRT1 activation decreased the proinflammatory effects induced by TNF-??. In addition, treatment of SIRT1 activator and overexpression of SIRT1 inhibited the expression and activation of the main proinflammatory regulator NF-??B, which was increased by TNF-??. When SIRT1 was overexpressed in chondrocytes, the anti-inflammatory action of SIRT1 was similar to that exerted by resveratrol. Conclusions: SIRT1 activation deacetylates and inactivates NF-??B, and thereby, exerts an anti-inflammatory effect on chondrocytes, suggesting that SIRT1 activators could be explored as potential treatments for arthritis. ? 2012 Osteoarthritis Research Society International.
机译：目的：进行本研究以阐明SIRT1信号传导在人关节软骨细胞关节炎症中的可能作用。设计：进行实时定量逆转录聚合酶链反应（qRT-PCR）和蛋白质印迹，以检测与肿瘤坏死因子有关的基因产物和蛋白质。 （TNF-α）诱导的人原代软骨细胞的炎症和软骨降解。通过明胶酶谱评估基质金属蛋白酶（MMP）-2和MMP-9活性。还进行了SIRT1的过表达和敲低研究，以研究SIRT1是否与软骨细胞中白藜芦醇的抗炎活性有关。结果：白藜芦醇剂量依赖性地抑制人软骨细胞中TNF-α诱导的环氧合酶-2（COX-2），MMP-1，MMP-3，MMP-13和PGE2的产生。此外，用TNF-α处理可增加MMP-2和MMP-9活性。然而，SIRT1的激活降低了TNF-α诱导的促炎作用。另外，SIRT1激活剂的处理和SIRT1的过表达抑制了主要促炎性调节剂NF-κB的表达和激活，而TNF-α则增加了它的表达和激活。当SIRT1在软骨细胞中过度表达时，SIRT1的抗炎作用类似于白藜芦醇。结论：SIRT1激活可以使NF-κB脱乙酰并失活，从而对软骨细胞发挥消炎作用，这表明SIRT1激活剂可作为治疗关节炎的潜在方法。 ？ 2012年国际骨关节炎研究学会。

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