Graduate School of Fisheries Science and Environmental Studies, Nagasaki University, Nagasaki, Japan.
Cell Factory Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea.
Phytother Res. 2018 Mar;32(3):452-458. doi: 10.1002/ptr.5988. Epub 2017 Dec 11.
Safe and efficient therapeutic agents for bone diseases are required in natural sources. We previously found that edible seaweed-derived polysaccharide porphyran exhibited anti-inflammatory effects through the down regulation of nuclear factor-κB. The aim of this study was to investigate the availability of porphyran as a therapeutic agent for bone diseases. The effects of porphyran on receptor activator of nuclear factor κB ligand (RANKL)-induced osteoclastogenesis in RAW264.7 cells were examined. Porphyran suppressed RANKL-induced osteoclast formation in a concentration-dependent manner (6.25-50 μg/ml) without any cytotoxic effects. Furthermore, real-time polymerase chain reaction analyses indicated that porphyran at 50 μg/ml significantly attenuated the RANKL-induced increase in the mRNA levels of osteoclastogenesis-related marker genes such as nuclear factor of activated T cells, tartrate-resistant acid phosphatase, cathepsin K, and matrix metalloproteinase-9 in RAW264.7 cells. To our knowledge, this is the first report showing that edible-seaweed-derived polysaccharide porphyran can suppress RANKL-induced osteoclastogenesis. Our results suggest that porphyran can be used as a safe therapeutic agent to improve osteoclast-related pathological conditions.
天然来源中需要安全有效的治疗骨疾病的药物。我们之前发现,可食用海藻衍生多糖卟啉通过下调核因子-κB 发挥抗炎作用。本研究旨在探讨卟啉作为治疗骨疾病的药物的可能性。研究了卟啉对 RAW264.7 细胞中核因子κB 受体激活剂配体(RANKL)诱导的破骨细胞生成的影响。结果表明,卟啉以浓度依赖性方式(6.25-50μg/ml)抑制 RANKL 诱导的破骨细胞形成,而没有任何细胞毒性作用。此外,实时聚合酶链反应分析表明,50μg/ml 的卟啉可显著减弱 RANKL 诱导的 RAW264.7 细胞中破骨细胞生成相关标记基因(如激活 T 细胞核因子、抗酒石酸酸性磷酸酶、组织蛋白酶 K 和基质金属蛋白酶-9)的 mRNA 水平的增加。据我们所知,这是第一项表明可食用海藻衍生多糖卟啉可抑制 RANKL 诱导的破骨细胞生成的报告。我们的结果表明,卟啉可用作安全的治疗剂来改善与破骨细胞相关的病理状况。