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首页> 外文期刊>Journal of cellular physiology. >Chitooligosaccharide inhibits RANKL-induced osteoclastogenesis and ligation-induced periodontitis by suppressing MAPK/ c-fos/NFATCl signaling
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Chitooligosaccharide inhibits RANKL-induced osteoclastogenesis and ligation-induced periodontitis by suppressing MAPK/ c-fos/NFATCl signaling

机译:Chitooligosaccharide抑制RANKL-inducedosteoclastogenesis和ligation-induced牙周炎通过抑制MAPK / c-fos / NFATCl信号

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摘要

Considering the high rate of osteoclast-related diseases worldwide, research targeting osteoclast formation/function is crucial. In vitro, we demonstrated that chitooligosaccharide (CS) dramatically inhibited osteoclastogenesis as well as osteoclast function dose-dependently. CS suppressed osteoclast-specific genes expression during osteoclastogenesis. Furthermore, we found that CS attenuated receptor activator of nuclear factor kappa B ligand (RANKL)-mediated mitogen-activated protein kinase (MAPK) pathway involving p38, erk1/2, and jnk, leading to the reduced expression of c-fos and nuclear factor of activated T cells c1 (NFATcl) during osteoclast differentiation. In vivo, we found CS protected rats from periodontitis-induced alveolar bone loss by micro-computerized tomography and histological analysis. Overall, CS inhibited RANKL-induced osteoclastogenesis and ligature-induced rat periodontitis model, probably by suppressing the MAPK/ c-fos/NFATc1 signaling pathway. Therefore, CS may be a safe and promising treatment for osteoclast-related diseases.
机译:考虑到osteoclast-related率高疾病在世界范围内,研究针对破骨细胞形成/函数是至关重要的。证明chitooligosaccharide (CS)显著抑制osteoclastogenesis破骨细胞功能存在剂量依赖的相关性。抑制osteoclast-specific基因表达在osteoclastogenesis。CS减毒受体激活核因子k B配体(RANKL)介导的增殖蛋白激酶(MAPK)途径涉及p38 erk1/2物,导致的c-fos和核因子的表达式在破骨细胞激活T细胞c1 (NFATcl)分化。老鼠从periodontitis-induced牙槽骨micro-computerized断层和损失组织学分析。RANKL-induced osteoclastogenesis和ligature-induced大鼠牙周炎模型,可能通过抑制MAPK / c-fos / NFATc1信号通路。并承诺osteoclast-related治疗疾病。

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