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首页> 外文会议>ASME bioengineering conference >NF-kB MEDIATES CARTILAGE DEGRADATION INDUCED BY TRAUMA INJURY AND INTERLEUKIN-1
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NF-kB MEDIATES CARTILAGE DEGRADATION INDUCED BY TRAUMA INJURY AND INTERLEUKIN-1

机译：NF-kB介导外伤和白细胞介素-1引起的软骨降解

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摘要

Chondrocyte death, induced by impact injury (necrosis) and/or apoptotic inducers such as cytokines, and high level of nitric oxide, is important for the development of post-traumatic arthritis (PTA). The upregulation of pro-inflammatory cytokines, such as interleukin -1 (IL-1) and Tumor necrosis factor (TNF) a, is known to mediate cartilage degradation in inflammatory diseases and after trauma injury. IL-1 induces the degradation of proteoglycan (PG) in cartilage through NF-kB and Mitogen-activated protein kinases (MAPK:p38, ERK and JNK) pathways. IL-1 is highly upregulated in synovial joint after impact injury, but the role of IL-1 induced chondrocyte death and matrix/PG degradation in injured cartilage is not completely clear.
机译：冲击损伤（坏死）和/或凋亡诱导物（例如细胞因子）和高水平的一氧化氮诱导的软骨细胞死亡对于创伤后关节炎（PTA）的发展很重要。已知促炎细胞因子，例如白介素-1（IL-1）和肿瘤坏死因子（TNF）a的上调介导了炎症疾病和创伤损伤后的软骨降解。 IL-1通过NF-kB和丝裂原激活的蛋白激酶（MAPK：p38，ERK和JNK）途径诱导软骨中蛋白聚糖（PG）的降解。 IL-1在冲击损伤后的滑膜关节中高度上调，但是IL-1诱导的软骨细胞死亡和基质/ PG降解在受伤的软骨中的作用尚不完全清楚。

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