Nitric oxide in inflammation and pain associated with osteoarthritis.
Nitric oxide in inflammation and pain associated with osteoarthritis.
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DOI：
10.1186/ar2463
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发表时间：
2008
影响因子：
4.9
通讯作者：
Abramson SB
中科院分区：
文献类型：
--
作者：
Abramson SB
骨关节炎（OA）是一种退行性疾病，涉及软骨细胞，软骨和其他关节组织，并有许多潜在的原因，包括生化和机械因素。虽然促炎因子包括一氧化氮（NO）与OA相关，但最近的证据表明NO及其氧化还原衍生物也可能在关节中发挥保护作用。然而，OA发生和发展的机制尚未完全了解。实验表明，NO在OA的发展中起分解代谢作用，并介导炎症反应，参与基质金属蛋白酶的降解，抑制胶原和蛋白多糖的合成，并有助于介导细胞凋亡。然而，也有证据表明，在培养的软骨细胞中，外源性NO的加入可能通过阻止转录因子核因子-κB的核定位来抑制促炎活化，而过氧亚硝酸盐-NO的氧化还原衍生物-的存在似乎通过维持核因子-κB的核定位来增强炎症反应。此外，在一定条件下，外源性NO可刺激培养的大鼠成纤维细胞和人肌腱细胞胶原合成。NO在多种细胞类型中的保护作用，沿着在培养的软骨细胞中的相反活性，表明NO可能在软骨细胞功能中发挥额外的保护作用。NO及其衍生物在伤害感受和疼痛中具有类似的复杂参与，这可能有助于OA的功能障碍。进一步的研究可能有助于阐明NO供体药物在OA管理中的潜在作用。
Osteoarthritis (OA) is a degenerative disease involving chondrocytes, cartilage and other joint tissues, and has a number of underlying causes, including both biochemical and mechanical factors. Although proinflammatory factors including nitric oxide (NO) are associated with OA, there is recent evidence suggesting that NO and its redox derivatives may also play protective roles in the joint. However, the mechanisms that underlie the development and progression of OA are not completely understood. Experiments have demonstrated that NO plays a catabolic role in the development of OA and mediates the inflammatory response, is involved in the degradation of matrix metalloproteinases, inhibits the synthesis of both collagen and proteoglycans, and helps to mediate apoptosis. However, there is also evidence that in cultured chondrocytes the addition of exogenous NO may inhibit proinflammatory activation by preventing the nuclear localization of the transcription factor nuclear factor-κB, whereas the presence of peroxynitrite – a redox derivative of NO – appears to enhance the inflammatory response by sustaining the nuclear localization of nuclear factor-κB. In addition, under some conditions exogenous NO can stimulate collagen synthesis in cultured rat fibroblasts and human tendon cells. The protective roles of NO in multiple cell types, along with the opposing activities in cultured chondrocytes, suggest that NO may play additional protective roles in chondrocyte function. NO and its derivatives have a similarly complicated involvement in nociception and pain, which may contribute to the functional disability of OA. Further research may help to elucidate a potential role for NO-donating agents in the management of OA.
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DOI：
10.1084/jem.182.6.2097
发表时间：
1995-12-01
期刊：
The Journal of experimental medicine
影响因子：
--
作者：
Amin AR;Di Cesare PE;Vyas P;Attur M;Tzeng E;Billiar TR;Stuchin SA;Abramson SB
通讯作者：
Abramson SB
影响因子：
2.8
作者：
Cherng, Yih-Giun;Chang, Hua-Chia;Chen, Ruei-Ming
通讯作者：
Chen, Ruei-Ming
影响因子：
158.5
作者：
Murad, Ferid
通讯作者：
Murad, Ferid
影响因子：
4
作者：
Mendes, AF;Caramona, MM;Lopes, MC
通讯作者：
Lopes, MC
影响因子：
3.4
作者：
Karan, A;Karan, MA;Öncel, A
通讯作者：
Öncel, A