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首页> 外文期刊>Journal of bone and mineral metabolism >Treatment with hydrogen molecules prevents RANKL-induced osteoclast differentiation associated with inhibition of ROS formation and inactivation of MAPK, AKT and NF-kappa B pathways in murine RAW264.7 cells
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Treatment with hydrogen molecules prevents RANKL-induced osteoclast differentiation associated with inhibition of ROS formation and inactivation of MAPK, AKT and NF-kappa B pathways in murine RAW264.7 cells

机译:氢分子处理可防止RANKL诱导的破骨细胞分化,这与抑制RAW264.7细胞中ROS的形成以及MAPK,AKT和NF-κB通路的失活有关。

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摘要

The bone protective effects of the hydrogen molecule (H_2) have been demonstrated in several osteoporosis models while the underlying molecular mechanism has remained unclear. Osteoclast differentiation is an important factor related to the pathogenesis of bone-loss related diseases. In this work, we evaluated the effects of incubation with H_2 on receptor activator of NFkB ligand (RANKL)-induced osteoclast differentiation. We found that treatment with H_2 prevented RANKL-induced osteoclast differentiation in RAW264.7 cells and BMMs. Treatment with H_2 inhibits the ability to form resorption pits of BMMs stimulated by RANKL. Treatment with H_2 reduced mRNA levels of osteoclast-specific markers including tartrate resistant acid phosphatase, calcitonin receptor, cathepsin K, metalloproteinase-9, carbonic anhydrase typell, and vacuolar-type H~+-ATPase.
机译:氢分子(H_2)的骨保护作用已在几种骨质疏松症模型中得到证实,而其潜在的分子机制仍不清楚。破骨细胞分化是与骨质流失相关疾病的发病机制有关的重要因素。在这项工作中,我们评估了H_2孵育对NFkB配体(RANKL)诱导的破骨细胞分化受体激活剂的影响。我们发现,H_2处理可防止RANKL诱导的RAW264.7细胞和BMM中的破骨细胞分化。 H_2处理抑制了RANKL刺激的BMM形成吸收凹坑的能力。 H_2处理可降低破骨细胞特异性标志物的mRNA水平,这些标志物包括抗酒石酸酸性磷酸酶,降钙素受体,组织蛋白酶K,金属蛋白酶9,碳酸酐酶typell和液泡型H〜-ATPase。

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