Effects of equol on apoptosis and proliferation of osteoblast through PI3K/AKT pathway in high glucose and high fat environment

Shuo LI; Xiangmin NI; Zhe XU; Wenyi ZHU; Xinyu LIANG; Jian WANG

doi:10.16016/j.2097-0927.202207184

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Effects of equol on apoptosis and proliferation of osteoblast through PI3K/AKT pathway in high glucose and high fat environment

Basic Medicine | 更新时间：2026-01-09

- Effects of equol on apoptosis and proliferation of osteoblast through PI3K/AKT pathway in high glucose and high fat environment
- Journal of Army Medical University Vol. 45, Issue 4, Pages: 349-357(2023)
- 作者机构：
  
  400037 重庆，陆军军医大学(第三军医大学)第二附属医院营养科
- 作者简介：
- 基金信息：
  
  the General Program of National Nature Science Foundation of China(81973040);the National Natural Science Foundation for Young Scholars of China(81602855)
- DOI：10.16016/j.2097-0927.202207184
  CLC： R151.41;R322.71;R587.2
- Received：28 July 2022，
  
  Revised：2022-11-19，
  
  Published：28 February 2023
- 稿件说明：
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Shuo LI, Xiangmin NI, Zhe XU, et al. Effects of equol on apoptosis and proliferation of osteoblast through PI3K/AKT pathway in high glucose and high fat environment[J]. Journal of Army Medical University, 2023, 45(4): 349-357.
DOI：

Shuo LI, Xiangmin NI, Zhe XU, et al. Effects of equol on apoptosis and proliferation of osteoblast through PI3K/AKT pathway in high glucose and high fat environment[J]. Journal of Army Medical University, 2023, 45(4): 349-357. DOI： 10.16016/j.2097-0927.202207184.

摘要

目的

探讨雌马酚(equol，Eq)对高糖高脂环境下成骨细胞增殖和凋亡的影响及其可能机制。

方法

建立ROS17/2.8成骨细胞高糖高脂损伤模型，设立对照组(C组)、模型组(M组)、不同浓度梯度Eq干预组(Eq

-7

组：1×10

-7

mol/L Eq，Eq

-6

组：1×10

-6

mol/L Eq，Eq

-5

组：1×10

-5

mol/L Eq)。药物处理24 h后，采用CCK-8、HE染色检测成骨细胞活性及形态结构变化，流式细胞术检测细胞凋亡及周期改变，Western blot检测细胞PI3K/AKT通路磷酸化程度及相关蛋白表达变化，并联合PI3K抑制剂验证PI3K/AKT通路在其中的作用。

结果

与C组比较，M组成骨细胞存活率降低、细胞抑制率增加(

0.05)，细胞形态结构明显损伤，细胞凋亡率增加(

0.05)，细胞周期G

期比例增加、S期比例降低(

0.05)，PI3K/AKT通路磷酸化程度降低、Cyclin D1、Bcl-2表达减少、Bax、cleaved caspase-3表达增加(

05)；与M组相比，各Eq干预组细胞存活率增加、细胞抑制率降低(

0.05)，细胞形态结构损伤减轻，细胞凋亡减少(

0.05)，细胞周期G

期比例降低、S期比例增加(

0.05)，PI3K/AKT通路磷酸化程度提高、Cyclin D1、Bcl-2表达增加、Bax、cleaved caspase-3表达减少(

0.05)，且Eq的干预效应随着浓度升高而增强；联合PI3K抑制剂后，Eq的上述效应显著降低。

结论

Eq可通过激活PI3K/AKT通路减少高糖高脂环境下成骨细胞凋亡、促进成骨细胞增殖。

Abstract

Objective

To explore the effect and mechanism of equol(Eq) on the proliferation and apoptosis of osteoblasts in high-glucose and high-fat environment.

Methods

High-glucose and high-fat model of ROS17/2.8 osteoblasts was established

and cells were divided into the control group (C group) and the model group (M group)

the Eq

-7

group (1×10

-7

mol/L Eq)

the Eq

-6

group(1×10

-6

mol/L Eq) and the Eq

-5

group(10

-5

mol/L Eq). CCK-8 assay and HE staining was used to detect the viability and morphology of osteoblasts; Flow cytometry was used to test the apoptosis and cell cycle; Western blotting was used to detect the phosphorylation of PI3K/AKT signaling pathway and expression of associated proteins of osteoblasts. PI3K inhibitor was added to confirm the role of PI3K/AKT signaling pathway in the osteoprotective effect of Eq.

Results

Compared with the C group

the cell structure of the M group was significantly damaged

the cell survival rate

proportion of S phase of cell cycle

the degree of phosphorylation of PI3K/AKT pathway

the expression of Cyclin D1 and Bcl-2 in the M group decreased

while cell inhibition rate

cell apoptosis

proportion of G

phase of cell cycle

the expression of Bax and cleaved caspase-3 of the M group increased (

0.05); Compared with the M group

the Eq groups had increased cell survival rate

decreased cell inhibition rate

enhanced fraction of osteobla

st in the S phase and decreased osteoblast apoptosis rate(

0.05). Eq treatment enhanced the phosphorylation of PI3K/AKT pathway of osteoblasts and increased expression level of Cyclin D1 and Bcl-2 protein and decreased expression of Bax and cleaved caspase-3 (

0.05). The intervention effect of Eq enhanced with the increase of concentration of Eq. However

this regulatory effect of Eq almost disappeared after co-administration of PI3K inhibitor.

Conclusion

Eq can reduce the apoptosis and promote the proliferation of osteoblasts in the high-glucose and high-fat environment by activating the PI3K/AKT pathway.

关键词

Keywords

references

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