Anti-inflammatory effects of IL-4 and dynamic compression in IL-1β stimulated chondrocytes
Anti-inflammatory effects of IL-4 and dynamic compression in IL-1β stimulated chondrocytes
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DOI：
10.1016/j.bbrc.2005.11.016
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发表时间：
2006-01-06
影响因子：
3.1
通讯作者：
Lee, DA
中科院分区：
文献类型：
--
作者：
Chowdhury, TT;Bader, DL;Lee, DA
机械负荷可通过抑制（NO）-N-来对抗IL-1 β诱导的炎症通路。和PGE（2），已知参与软骨降解的分解代谢介质。目前的研究调查了动态压缩与抗炎细胞因子IL-4组合以进一步消除IL-1 β诱导的效应的潜力。所提供的数据表明，在存在和不存在IL-1 β的情况下，单独的IL-4可以抑制亚硝酸盐的释放，并部分逆转IL-1 β诱导的PGE（2）释放。当IL-4和动态加压联合使用时，可进一步消除IL-1 β诱导的亚硝酸盐和PGE（2）的释放。IL-1 β抑制[H-3]胸苷掺入，IL-4或动态应变单独或两者联合可逆转这种作用。相比之下，在IL-1 β刺激的构建体中，（SO 4）-S-35掺入不受IL-4和/或动态应变的影响。因此，IL-4和机械负荷可能为OA中观察到的软骨破坏提供潜在的保护机制。(c)2005年爱思唯尔公司All rights reserved.
Mechanical loading can counteract inflammatory pathways induced by IL-1 beta by inhibiting (NO)-N-. and PGE(2), catabolic mediators known to be involved in cartilage degradation. The current study investigates the potential of dynamic compression, in combination with the anti-inflammatory cytokine, IL-4, to further abrogate the IL-1 beta induced effects. The data presented demonstrate that IL-4 alone can inhibit nitrite release in the presence and absence of IL-1 beta and partially reverse the IL-1 beta induced PGE(2) release. When provided in cornbination, IL-4 and dynamic compression Could further abrogate the IL-1 beta induced nitrite and PGE(2) release. IL-1 beta inhibited [H-3]thymidine incorporation and this effect could be reversed by IL-4 or dynamic strain alone or both in combination. By contrast, (SO4)-S-35 incorporation was not influenced by IL-4 and/or dynamic strain in IL-1 beta stimulated constructs. IL-4 and mechanical loading may therefore provide a potential protective mechanism for cartilage destruction as observed in OA. (c) 2005 Elsevier Inc. All rights reserved.