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首页> 外文期刊>Cellular Physiology and Biochemistry >Quercetin triggers apoptosis of lipopolysaccharide (LPS)-induced osteoclasts and inhibits bone resorption in RAW264.7 cells
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Quercetin triggers apoptosis of lipopolysaccharide (LPS)-induced osteoclasts and inhibits bone resorption in RAW264.7 cells

机译：槲皮素触发脂多糖（LPS）诱导的破骨细胞凋亡并抑制RAW264.7细胞的骨吸收

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Aims: Quercetin, a flavonoid present in vegetables, has anti-inflammatory properties and potential inhibitory effects on bone resorption. Up to date, the effect of quercetin on lipopolysaccharide (LPS)-induced osteoclastogenesis has not yet been reported. In the current study, we evaluated the effect of quercetin on LPS-induced osteoclast apoptosis and bone resorption. Methods: RAW264.7 cells were non-treated, treated with LPS alone, or treated with both LPS and quercetin. After treatment, the number of osteoclasts, cell viability, bone resorption and osteoclast apoptosis were measured. The expressions of osteoclast-related genes including tartrate-resistant acid phosphatase (TRAP), matrix metalloproteinase-9 (MMP9) and cathepsin K (CK) were determined by real-time quantitative polymerase chain reaction (qPCR). Protein levels of receptor activator of nuclear factor-κB (RANK), tumor necrosis factor receptor-associated factor 6 (TRAF6), cyclooxygenase-2 (COX-2), Bax, Bcl-2 and mitogenactivated protein kinases (MAPKs) were measured using Western blotting assays. The MAPK signaling pathway was blocked by pretreatment with MAPK inhibitors. Results: LPS directly promoted osteoclast differentiation of RAW264.7 cells and upregulated the protein expression of RANK, TRAF6 and COX-2; while quercetin significantly decreased the number of LPS-induced osteoclasts in a dose-dependent manner. None of the treatments increased cytotoxicity in RAW264.7 cells. Quercetin inhibited mRNA expressions of osteoclast-related genes and protein levels of RANK, TRAF6 and COX-2 in LPS-induced mature osteoclasts. Quercetin also induced apoptosis and inhibited bone resorptive activity in LPS-induced mature osteoclasts. Furthermore, quercetin promoted the apoptotic signaling pathway including increasing the phosphorylation of p38-MAPK, c-Jun N-terminal kinases/stress-activated protein kinases.
机译：目的：槲皮素，一种存在于蔬菜中的类黄酮，具有抗炎特性，并且对骨吸收具有潜在的抑制作用。迄今为止，尚未报道槲皮素对脂多糖（LPS）诱导的破骨细胞形成的作用。在当前的研究中，我们评估了槲皮素对LPS诱导的破骨细胞凋亡和骨吸收的影响。方法：RAW264.7细胞未经处理，单独使用LPS处理或同时使用LPS和槲皮素处理。治疗后，测量破骨细胞的数量，细胞活力，骨吸收和破骨细胞凋亡。通过实时定量聚合酶链反应（qPCR）测定破骨细胞相关基因的表达，包括抗酒石酸酸性磷酸酶（TRAP），基质金属蛋白酶9（MMP9）和组织蛋白酶K（CK）。使用以下方法测量核因子-κB（RANK），肿瘤坏死因子受体相关因子6（TRAF6），环氧合酶2（COX-2），Bax，Bcl-2和促分裂原活化蛋白激酶（MAPK）的受体激活蛋白的蛋白水平。蛋白质印迹分析。 MAPK抑制剂预处理可阻断MAPK信号通路。结果：脂多糖直接促进RAW264.7细胞的破骨细胞分化，并上调RANK，TRAF6和COX-2的蛋白表达。槲皮素以剂量依赖性方式显着减少LPS诱导的破骨细胞的数量。没有一种疗法能增加RAW264.7细胞的细胞毒性。槲皮素抑制LPS诱导的成熟破骨细胞中破骨细胞相关基因的mRNA表达以及RANK，TRAF6和COX-2的蛋白水平。槲皮素还可以在LPS诱导的成熟破骨细胞中诱导细胞凋亡并抑制骨吸收活性。此外，槲皮素促进了细胞凋亡的信号通路，包括增加p38-MAPK，c-Jun N端激酶/应激激活的蛋白激酶的磷酸化。

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