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The use of apocynin inhibits osteoclastogenesis

机译:Apocynin的使用抑制了骨髓细胞发生

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Abstract Reactive oxygen species (ROS) are produced by NADPH oxidase (NOX), an enzyme that reduces oxygen by using NADPH as a substrate. Apocynin (APO) is a catechol that is used as a NOX inhibitor, and N‐acetyl‐cysteine ??(NAC) can reduce intracellular ROS levels. In this work, the effect of APO and NAC on osteoclast formation were evaluated. APO and NAC significantly decreased the number of tartrate‐resistant acid phosphatase (TRAP)‐positive cells and the osteoclast area. We analyzed bone‐marrow derived monocyte‐macrophages (BMMs) that differentiated into osteoclasts after RANKL stimulation. Stimulation was associated with either APO or NAC treatment and osteoclastogenesis marker expression, including NFATc1, MMP‐9, and DC‐STAMP, was evaluated. APO decreased the intracellular calcium concentration by calcium channels other than ITPR1 and TPC2. On the other hand, APO reduced Tnfrsf11a (RANK) expression and did not alter Fam102a (EEIG1) expression. Therefore, our results demonstrate that APO inhibits osteoclastogenesis by the RANK‐RANKL‐related signaling pathways, decreases osteoclast markers, and reduces intracellular calcium concentration.
机译:摘要通过NADPH氧化酶(NOx)制备了反应性氧物质(ROS),一种通过使用NADPH作为基材来减少氧的酶。 Apocynin(APO)是一种用作NOx抑制剂的儿茶酚,N-乙酰基半胱氨酸(NAc)可以降低细胞内ROS水平。在这项工作中,评估APO和NAC对破骨细胞形成的影响。 APO和NAC显着降低了抗酒石酸酸磷酸酶(捕集性)和破骨细胞面积的抗性酸性磷酸酶(捕集性)的数量。我们分析了骨髓衍生的单核细胞 - 巨噬细胞(BMMS),其在RANKL刺激后分化成骨细胞。刺激与APO或NAC治疗相关,并评估骨髓细胞发生标志物表达,包括NFATC1,MMP-9和DC印记。 APO通过除ITPR1和TPC2之外的钙通道降低细胞内钙浓度。另一方面,APO减少了TNFRSF11a(等级)表达,并没有改变FAM102A(EEIG1)表达。因此,我们的结果表明,APO通过秩-Rankl相关的信号通路抑制骨细胞发生,降低破骨细胞标志物,降低细胞内钙浓度。

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