| 四烯甲萘醌保护成骨细胞氧化损伤的作用研究 |
| 投稿时间：2020-05-18 修订日期：2020-07-13 点此下载全文 |
| 引用本文：蒋益忠,林丽娟,辛海量,金玉娥,蒋益萍,薛黎明.四烯甲萘醌保护成骨细胞氧化损伤的作用研究[J].药学实践杂志,2020,38(6):523~527 |
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| 基金项目:上海市卫生和计划生育委员会面上项目(201740068)；海军军医大学本科创新孵化基地项目(PH2019102) |
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| 中文摘要:目的 考察四烯甲萘醌(MK4)对成骨细胞氧化损伤的保护作用，阐明MK4防治骨质疏松作用机制。方法 采用过氧化氢(H2O2)刺激小鼠成骨细胞系（MC3T3-E1）氧化应激模型，考察细胞活力、ALP活性和骨结节面积，DCFH-DA法检测活性氧(ROS)水平，JC-1检测线粒体膜电势，Annexin V-FITC/PI法检测细胞凋亡率，RT-PCR法考察氧化应激相关基因FoxO1、FoxO3、SOD、Bcl-2和bax等的mRNA表达。结果 10 μmol/L四烯甲萘醌能显著提高H2O2刺激的成骨细胞增殖、ALP活性、骨结节形成面积和增强细胞膜电势，显著降低H2O2刺激的成骨细胞内丙二醛和活性氧水平，同时显著降低成骨细胞凋亡率和细胞凋亡因子bax/Bcl-2的mRNA表达水平，显著提高抗氧化酶SOD和转录因子FoxO1、FoxO3的mRNA表达。结论 四烯甲萘醌可通过调控FoxO通路保护成骨细胞氧化损伤和通过下调bax/Bcl-2比例，降低成骨细胞凋亡。 |
| 中文关键词:四烯甲萘醌 骨质疏松 成骨细胞 氧化损伤 FoxO通路 |
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| Study on the protective effect of menatetrenone against the oxidative stress of osteoblasts |
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| Abstract:Objective To investigate the protective effect of menatetrenone (MK4) on the osteoblasts in oxidative stress, and to clarify the anti-osteoporosis mechanism of MK4.Methods Mouse osteoblasts (MC3T3-E1) induced by hydrogen peroxide (H2O2) was used. Cell viability, ALP activity and the area of bone nodule were observed. The level of ROS was detected by DCFH-DA, mitochondrial membrane potential by JC-1, apoptosis rate by annexin V-FITC/PI, and the expression of FoxO1, FoxO3, SOD, bcl-2 and bax by RT-PCR.Results Menatetrenone at 10 μmol/L significantly increased the proliferation of osteoblasts stimulated by H2O2, ALP activity, bone nodule formation area, cell membrane potential, the antioxidant SOD and transcription factors FoxO1 and FoxO3 mRNA expression. In the meantime, the elevated malondialdehyde and reactive oxygen species level in cells induced by H2O2, the apoptosis rate and the mRNA expression level of bax/Bcl-2 were significantly reduced.Conclusion menatetrenone can protect osteoblasts from oxidative damage by regulating FoxO pathway and reduce osteoblasts apoptosis by up regulating the proportion of Bcl-2/bax. |
| keywords:menatetrenone osteoporosis osteoblasts oxidative stress FoxO pathway |
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