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首页> 外文期刊>Journal of Cellular Physiology >Enhanced fracture repair by leukotriene antagonism is characterized by increased chondrocyte proliferation and early bone formation: a novel role of the cysteinyl LT-1 receptor.
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Enhanced fracture repair by leukotriene antagonism is characterized by increased chondrocyte proliferation and early bone formation: a novel role of the cysteinyl LT-1 receptor.

机译：增强骨折修复白三烯对抗特点是增加了软骨细胞核扩散和早期的骨形成:一本小说作用的半胱氨酰LT-1受体。

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摘要

Inflammatory mediators and drugs which affect inflammation can influence the healing of injured tissues. Leukotrienes are potent inflammatory mediators, and similar to prostaglandins, are metabolites of arachidonic acid which can have positive or negative effects on bone and cartilage tissues. Here we tested the hypothesis that blocking the negative regulation of leukotrienes, would lead to enhanced endochondral bone formation during fracture repair. A closed femoral fracture was created in mice. Animals were divided into three groups for treatment with either montelukast sodium, a cysteinyl leukotriene type 1 receptor antagonist (trade name Singulair), zileuton, a 5-lipoxygenase enzyme inhibitor (trade name Zyflo), or carrier alone. The fractures were analyzed using radiographs, quantitative gene expression, histology and histomorphometry, and immunohistochemistry. Both the montelukast sodium group and the zileuton group exhibited enhanced fracture repair when compared with controls. Both treatment groups exhibited increased callous size and earlier bone formation when compared to controls as early as day 7. Gene expression analysis of treatment groups showed increased markers of chondrocyte proliferation and differentiation, and increased early bone formation markers when compared with controls. Treatment with montelukast sodium directly targeted the cysteinyl leukotriene type 1 receptor, leading to increased chondrocyte proliferation at early time points. These novel findings suggests a potential mechanism by which the cysteinyl leukotriene type 1 receptor acts as a negative regulator of chondrocyte proliferation, with important and previously unrecognized implications for both fracture repair, and in a broader context, systemic chondrocyte growth and differentiation.
机译：炎症介质和药物的影响炎症会影响治疗的受伤组织。介质,类似于前列腺素的花生四烯酸代谢物对骨骼和积极或消极的影响软骨组织。阻塞的负调控白细胞三烯,会导致增强软骨内在骨折修复骨形成。股骨骨折成立于老鼠。被分成三个组治疗montelukast钠,半胱氨酰1型白三烯受体拮抗剂(贸易5-lipoxygenase名顺尔宁),与酶抑制剂(贸易名称欣),或载体一个人。射线照片,定量基因表达,组织学和histomorphometry,免疫组织化学。组和与组表现出增强的骨折修复与控制相比。治疗组表现出冷酷的大小增加和之前相比骨形成控制早在第七天。分析治疗组显示增加软骨细胞增殖和标记早期骨分化,增加形成标记相比,控制。直接montelukast钠治疗针对半胱氨酰白三烯1型受体,导致软骨细胞增加扩散在早期的时间点。研究结果表明潜在的机制1型的半胱氨酰白三烯受体作为消极的软骨细胞的监管机构扩散,重要的和识别裂缝的影响修复、在更广泛的背景下,系统性软骨细胞生长和分化。

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