Suh Kwang Sik, Choi Eun-Mi, Kwon Mikwang, Chon Suk, Oh Seungjoon, Woo Jeong-Taek, Kim Sung Woon, Kim Jin-Woo, Kim Young Seol
Department of Endocrinology and Metabolism, Kyung Hee University School of Medicine, Republic of Korea.
Biol Pharm Bull. 2009 Apr;32(4):746-9. doi: 10.1248/bpb.32.746.
Reducing sugar, 2-deoxy-D-ribose (dRib), produces reactive oxygen species through autoxidation and protein glycosylation and causes osteoblast dysfunction. Kaempferol, a natural flavonoid, was investigated to determine whether it could influence dRib-induced cellular dysfunction and oxidative cell damage in the MC3T3-E1 mouse osteoblastic cell line. Osteoblastic cells were treated with 30 mM dRib in the presence or absence of kaempferol (10(-9)-10(-5) M) and markers of osteoblast function and lipid peroxidation were subsequently examined. Kaempferol (10(-9)-10(-5) M) significantly inhibited the dRib-induced decrease in growth of MC3T3-E1 osteoblastic cells. In addition, treatment with kaempferol resulted in a significant elevation of alkaline phosphatase (ALP) activity, collagen content, and mineralization in the cells. Treatment with kaempferol increased osteoprotegerin (OPG) secretion and decreased malondialdehyde (MDA) contents of MC3T3-E1 osteoblastic cells in the presence of 30 mM dRib. Taken together, these results suggest that kaempferol inhibits dRib-induced osteoblastic cell damage and may be useful for the treatment of diabetes-related bone disease.
还原糖2-脱氧-D-核糖（dRib）通过自氧化和蛋白质糖基化产生活性氧，导致成骨细胞功能障碍。研究了天然黄酮类化合物山奈酚，以确定其是否能影响dRib诱导的MC3T3-E1小鼠成骨细胞系细胞功能障碍和氧化细胞损伤。在存在或不存在山奈酚（10^(-9)-10^(-5) M）的情况下，用30 mM dRib处理成骨细胞，随后检测成骨细胞功能和脂质过氧化的标志物。山奈酚（10^(-9)-10^(-5) M）显著抑制dRib诱导的MC3T3-E1成骨细胞生长下降。此外，用山奈酚处理导致细胞中碱性磷酸酶（ALP）活性、胶原蛋白含量和矿化显著升高。在存在30 mM dRib的情况下，用山奈酚处理增加了MC3T3-E1成骨细胞的骨保护素（OPG）分泌并降低了丙二醛（MDA）含量。综上所述，这些结果表明山奈酚可抑制dRib诱导的成骨细胞损伤，可能对治疗糖尿病相关骨病有用。
