Department of Pharmaceutical Engineering, Soonchunhyang University, Asan 31538, Republic of Korea.
Department of Food and Nutrition, College of Medical and Life Science, Silla University, Busan 46958, Republic of Korea.
Fitoterapia. 2021 Jul;152:104921. doi: 10.1016/j.fitote.2021.104921. Epub 2021 May 11.
Accumulating evidence has shown an association between osteoporosis and oxidative damage. In the present study, the protective effects of diphlorethohydroxycarmalol (DPHC) isolated from the brown algae Ishige okamurae against HO-induced oxidative damage via bone morphogenetic protein 2 (BMP2)/ runt-related transcription factor 2 (Runx2) signaling were investigated using MC3T3-E1 osteoblastic cells. DPHC counteracted the reduction in cell viability caused by HO exposure and protected against HO-induced dysfunction, demonstrated by improved cellular alkaline phosphatase (ALP) activity and calcium deposition. In addition, treatment with 0.05-0.2 mM DPHC elevated the protein expression of osteoblast differentiation factors type 1 collagen, ALP, p-Smad1/5, Osterix, BMP2, and Runx2, in response to HO-induced oxidative damage. Importantly, DPHC decreased the expression levels of receptor activator of nuclear factor kappa-B ligand, which promotes bone resorption, and inhibited the HO-induced generation of reactive oxygen species. Taken together, the results suggest that DPHC counteracts the effects of oxidative stress in osteoblastic cells and has the potential to be effective in preventing and alleviating osteoporosis.
越来越多的证据表明，骨质疏松症与氧化损伤之间存在关联。在本研究中，使用 MC3T3-E1 成骨细胞研究了从褐藻 Ishige okamurae 中分离出的二氢二羟基卡玛醇 (DPHC) 通过骨形态发生蛋白 2 (BMP2)/ runt 相关转录因子 2 (Runx2) 信号对 HO 诱导的氧化损伤的保护作用。DPHC 抵消了 HO 暴露引起的细胞活力降低，并防止了 HO 诱导的功能障碍，表现为细胞碱性磷酸酶 (ALP) 活性和钙沉积的改善。此外，用 0.05-0.2 mM DPHC 处理可提高成骨分化因子 1 型胶原、ALP、p-Smad1/5、Osterix、BMP2 和 Runx2 的蛋白表达，以应对 HO 诱导的氧化损伤。重要的是，DPHC 降低了核因子 kappa-B 配体受体激活剂的表达水平，该配体促进骨吸收，并抑制 HO 诱导的活性氧的产生。总之，这些结果表明，DPHC 可抵抗成骨细胞中氧化应激的影响，并有潜力预防和缓解骨质疏松症。
