Alpha-Lipoic Acid Alleviates High-Glucose Suppressed Osteogenic Differentiation of MC3T3-E1 Cells via Antioxidant Effect and PI3K/Akt Signaling Pathway

Alpha-Lipoic Acid Alleviates High-Glucose Suppressed Osteogenic Differentiation of MC3T3-E1 Cells via Antioxidant Effect and PI3K/Akt Signaling Pathway
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DOI:
10.1159/000479605
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发表时间:
2017-01-01
影响因子:
--
通讯作者:
Liu, Zhonghao
Liu, Zhonghao
中科院分区:
医学1区
文献类型:
--
作者:
Dong, Kai;Hao, Pengjie;Liu, Zhonghao

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背景/目的:糖尿病患者种植体失败的风险较高。一个主要原因是高糖诱导的氧化应激。α -硫辛酸(ALA)是一种天然存在的化合物和膳食补充剂,已被确定为一种有效的抗氧化剂,是一种强大的自由基清除剂。然而,关于ALA对高糖培养成骨细胞成骨分化影响的研究尚少。本研究旨在探讨ALA对高糖条件下MC3T3-E1细胞成骨分化的影响。方法:将MC3T3-E1细胞分为正常葡萄糖(5.5 mM)组(对照)、高糖(25.5 mM)组、高糖+ 0.1 mM ALA组、高糖+ 0.2 mM ALA组。采用MTT法、碱性磷酸酶(ALP)活性法、茜素红染色法和实时聚合酶链反应法观察细胞的增殖、成骨分化和矿化情况。还通过活性氧(ROS)和超氧化物歧化酶(SOD)的产生来评估高糖诱导的氧化损伤。Western blot检测PI3K/Akt通路的作用。结果:高糖诱导的ROS显著抑制MC3T3-E1细胞的增殖、成骨分化和矿化。ALA对小鼠氧化损伤和成骨功能障碍均有抑制作用。此外,ALA激活了PI3K/Akt通路。结论:我们证明ALA可能通过抗氧化作用和调节PI3K/Akt通路来减弱高糖介导的MC3T3-E1细胞功能障碍。(C) 2017作者:s . Karger AG,巴塞尔出版
Background/Aims: Patients with diabetes mellitus have a higher risk of dental implant failure. One major cause is high-glucose induced oxidative stress. Alpha-lipoic acid (ALA), a naturally occurring compound and dietary supplement, has been established as a potent antioxidant that is a strong scavenger of free radicals. However, few studies have yet investigated the effect of ALA on osteogenic differentiation of osteoblasts cultured with high glucose medium. The aim of this study is to investigate the effects of ALA on the osteoblastic differentiation in MC3T3-E1 cells under high glucose condition. Methods: MC3T3-E1 cells were divided into 4 groups including normal glucose (5.5 mM) group (control), high glucose (25.5 mM) group, high glucose + 0.1 mM ALA group, and high glucose + 0.2 mM ALA group. The proliferation, osteogenic differentiation and mineralization of cells were evaluated by MTT assay, alkaline phosphatase (ALP) activity assay, alizarin red staining and real time-polymerase chain reaction. High-glucose induced oxidative damage was also assessed by the production of reactive oxygen species (ROS) and superoxide dismutase (SOD). Western blots were performed to examine the role of PI3K/Akt pathway. Results: The proliferation, osteogenic differentiation and mineralization of MC3T3-E1 cells were significantly decreased by the ROS induced by high-glucose. All observed oxidative damage and osteogenic dysfunction induced were inhibited by ALA. Moreover, the PI3K/Akt pathway was activated by ALA. Conclusions: We demonstrate that ALA may attenuate high-glucose mediated MC3T3-E1 cells dysfunction through antioxidant effect and modulation of PI3K/Akt pathway. (C) 2017 The Author(s) Published by S. Karger AG, Basel