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浓缩生长因子通过 PI3K/Akt 信号通路调节高糖诱导的 MC3T3-E1 细胞成骨功能障碍。

Concentrate Growth Factors Regulate Osteogenic Dysfunction of MC3T3-E1 Cells Induced by High Glucose Through PI3K/Akt Signaling Pathway.

机构信息

PhD Student, Department of Implant Dentistry, School of Stomatology, Shandong University, Jinan, China.

Associate Chief Physician, Department of Dental Implantology, Yantai Stomatological Hospital, Yantai, China.

出版信息

Implant Dent. 2019 Oct;28(5):478-483. doi: 10.1097/ID.0000000000000921.

Abstract

INTRODUCTION

The aim of this study is to investigate the effects of Concentrate Growth Factors Extract (CGF-e) on the proliferation and osteogenic differentiation of MC3T3-E1 cells under high glucose condition.

MATERIALS AND METHODS

MC3T3-E1 cells were divided into 4 groups including normal glucose (5.5-mM) group (control), high glucose (25.5-mM) group, normal glucose + CGF-e group, and high glucose + CGF-e group. The proliferation, osteogenic differentiation and mineralization of osteoblasts were evaluated, respectively, by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, cytoskeleton analysis, alkaline phosphatase activity assay, alizarin red staining, and real-time polymerase chain reaction. Western blots analysis was used to explore the role of PI3K/Akt pathway.

RESULTS

The viability, osteogenic differentiation, and mineralization of MC3T3-E1 cells were significantly decreased by high glucose. All observed osteogenic dysfunction were inhibited by CGF-e. Moreover, the PI3K/Akt pathway was activated by CGF-e.

CONCLUSIONS

It was concluded that the soluble factors released by CGF could significantly attenuate high glucose-mediated MC3T3-E1 cells osteogenic dysfunction through the PI3K/Akt pathway.

摘要

简介

本研究旨在探讨浓缩生长因子提取物(CGF-e)在高糖条件下对 MC3T3-E1 细胞增殖和成骨分化的影响。

材料与方法

将 MC3T3-E1 细胞分为 4 组,包括正常葡萄糖(5.5-mM)组(对照组)、高葡萄糖(25.5-mM)组、正常葡萄糖+CGF-e 组和高葡萄糖+CGF-e 组。通过 3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐(MTT)测定法、细胞骨架分析、碱性磷酸酶活性测定、茜素红染色和实时聚合酶链反应分别评估成骨细胞的增殖、成骨分化和矿化。Western blot 分析用于探讨 PI3K/Akt 通路的作用。

结果

高葡萄糖显著降低了 MC3T3-E1 细胞的活力、成骨分化和矿化。CGF-e 抑制了所有观察到的成骨功能障碍。此外,CGF-e 激活了 PI3K/Akt 通路。

结论

可溶性 CGF 因子可通过 PI3K/Akt 通路显著减轻高糖介导的 MC3T3-E1 细胞成骨功能障碍。

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