Effects of ω3- and ω6-polyunsaturated fatty acids on RANKL-induced osteoclast differentiation of RAW264.7 cells: a comparative in vitro study.
Effects of ω3- and ω6-polyunsaturated fatty acids on RANKL-induced osteoclast differentiation of RAW264.7 cells: a comparative in vitro study.
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DOI：
10.3390/nu6072584
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发表时间：
2014-07-09
期刊：
影响因子：
5.9
通讯作者：
Coetzee M
中科院分区：
文献类型：
--
作者：
Boeyens JC;Deepak V;Chua WH;Kruger MC;Joubert AM;Coetzee M
据报道，多不饱和脂肪酸（PUFAs）在体内对骨具有合成代谢作用，但在ω3-和ω6-PUFAs中鉴定破骨细胞形成抑制剂的比较研究仍然缺乏。本研究评估了ω3-PUFAs、二十碳五烯酸（EPA）和二十二碳六烯酸（DHA）以及ω6-PUFAs、花生四烯酸（AA）和γ-亚麻酸（GLA）对RAW264.7破骨细胞分化模型的影响。通过计数酒石酸抗性酸性磷酸酶（TRAP）阳性的多核细胞来评估PUFAs对rankl诱导的破骨细胞形成的影响。PUFAs以剂量依赖性的方式显著抑制rankl诱导的破骨细胞形成，其中AA-和dha介导的抑制作用最强。此外，rankl诱导的关键破骨基因组织蛋白酶K和TRAP的mRNA和蛋白表达被AA和DHA更有效地抑制。由于DHA和AA抑制了破骨细胞的形成，在模拟骨板上观察，这些细胞的肌动蛋白环形成和骨吸收活性严重受损。因此，在所测试的PUFAs中，AA和DHA对rankl诱导的破骨细胞形成的抑制作用最有效，后者的抑制作用最强。总的来说，这些数据表明，这些PUFAs可能在调节以破骨细胞活性过度为特征的骨病中发挥重要作用。
Polyunsaturated fatty acids (PUFAs) have been reported to have an anabolic effect on bone in vivo, but comparative studies to identify inhibitors of osteoclast formation amongst ω3- and ω6-PUFAs are still lacking. Here we assessed the effects of the ω3-PUFAs, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and the ω6-PUFAs, arachidonic acid (AA) and γ-linolenic acid (GLA) on a RAW264.7 osteoclast differentiation model. The effects of PUFAs on RANKL-induced osteoclast formation were evaluated by counting tartrate resistant acid phosphatase (TRAP)-positive multinucleated cells. PUFAs significantly inhibited RANKL-induced osteoclast formation in a dose-dependent manner with AA- and DHA-mediated inhibition being the strongest. Furthermore, RANKL-induced mRNA- and protein expression of the key osteoclastogenic genes cathepsin K and TRAP were inhibited by AA and more potently by DHA. Owing to the attenuated osteoclastogenesis by DHA and AA, actin ring formation and bone resorptive activity of these cells as evaluated on bone-mimetic plates were severely compromised. Hence, of the tested PUFAs, AA and DHA were found to be the most effective in inhibiting RANKL-induced osteoclast formation with the latter providing the strongest inhibitory effects. Collectively, the data indicates that these PUFAs may play an important role in regulating bone diseases characterized by excessive osteoclast activity.
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