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红花提取物可预防 H2O2 诱导的成骨细胞 MC3T3-E1 功能障碍和氧化损伤。

Carthamus tinctorius flower extract prevents H2O2-induced dysfunction and oxidative damage in osteoblastic MC3T3-E1 cells.

机构信息

Plant Resources Research Institute, Duksung Women's University, Seoul, Korea.

出版信息

Phytother Res. 2010 Jul;24(7):1037-41. doi: 10.1002/ptr.3070.

Abstract

The flowers of Carthamus tinctorius L. (Compositae) have been widely used for enhancing blood circulation and postmenopausal disorder in women. In the present study, the potential protective effects of C. tinctorius flower extract (CFE) against reactive oxygen species (ROS) induced osteoblast dysfunction were investigated using osteoblastic MC3T3-E1 cells. The osteoblast function was assessed by measuring alkaline phosphatase activity, collagen content, calcium deposition, and RANKL production, and the oxidative status was assessed by measuring intracellular lipid peroxidation, and protein oxidation in osteoblastic MC3T3-E1 cells. A significant reduction in the alkaline phosphatase activity, collagen, and calcium deposition and an increase in the production of receptor activator of nuclear factor-kB ligand (RANKL) were observed after 0.3 mM H(2)O(2) addition. The H(2)O(2)-induced alterations were prevented by pre-incubating the osteoblasts with 2-10 microg/ml CFE for 48 h. When the oxidative stress was induced by H(2)O(2), the increased production of protein carbonyl and malondialdehyde was also reduced at the same CFE concentration. These results demonstrate that C. tinctorius flower can act as a biological antioxidant in a cell culture experimental model and protect osteoblasts from oxidative stress-induced toxicity.

摘要

红花(菊科)已被广泛用于改善血液循环和女性绝经后紊乱。本研究以成骨细胞 MC3T3-E1 细胞为模型,探讨红花提取物(CFE)对活性氧(ROS)诱导的成骨细胞功能障碍的潜在保护作用。通过测量碱性磷酸酶活性、胶原蛋白含量、钙沉积和核因子κB 受体激活剂配体(RANKL)的产生来评估成骨细胞功能,通过测量成骨细胞 MC3T3-E1 细胞内的脂质过氧化和蛋白氧化来评估氧化状态。加入 0.3mM H2O2 后,碱性磷酸酶活性、胶原蛋白和钙沉积显著降低,核因子κB 受体激活剂配体(RANKL)的产生增加。用 2-10μg/ml CFE 预处理成骨细胞 48h 可预防 H2O2 引起的变化。当 H2O2 诱导氧化应激时,同一 CFE 浓度下,蛋白羰基和丙二醛的产生也减少。这些结果表明,红花在细胞培养实验模型中可作为一种生物抗氧化剂,保护成骨细胞免受氧化应激诱导的毒性。

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