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雌马酚通过PI3K/AKT通路对高糖高脂环境下成骨细胞凋亡及增殖的影响
Effects of equol on apoptosis and proliferation of osteoblast through PI3K/AKT pathway in high glucose and high fat environment
- 陆军军医大学学报 2023年45卷第4期 页码：349-357
- 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：
[ 王建，E-mail: wj_xqhospital@163.com WANG Jian, E-mail: wj_xqhospital@163.com
- 基金信息：国家自然基金面上项目(81973040);国家自然基金青年科学基金项目(81602855)
DOI：10.16016/j.2097-0927.202207184
中图分类号： R151.41;R322.71;R587.2收稿：2022-07-28，
修回：2022-11-19，
纸质出版：2023-02-28
- 稿件说明：
移动端阅览
李硕, 倪向敏, 徐喆, 等. 雌马酚通过PI3K/AKT通路对高糖高脂环境下成骨细胞凋亡及增殖的影响[J]. 陆军军医大学学报, 2023,45(4):349-357.
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.
李硕, 倪向敏, 徐喆, 等. 雌马酚通过PI3K/AKT通路对高糖高脂环境下成骨细胞凋亡及增殖的影响[J]. 陆军军医大学学报, 2023,45(4):349-357. DOI： 10.16016/j.2097-0927.202207184.
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
2
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
2
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
2
与C组比较，M组成骨细胞存活率降低、细胞抑制率增加(
P
<
0.05)，细胞形态结构明显损伤，细胞凋亡率增加(
P
<
0.05)，细胞周期G
1
期比例增加、S期比例降低(
P
<
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(
P
<
0.
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(
P
<
0.05)，细胞形态结构损伤减轻，细胞凋亡减少(
P
<
0.05)，细胞周期G
1
期比例降低、S期比例增加(
P
<
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(
P
<
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
2
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
2
To explore the effect and mechanism of equol(Eq) on the proliferation and apoptosis of osteoblasts in high-glucose and high-fat environment.
Methods
2
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
2
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
1
phase of cell cycle
the expression of Bax and cleaved caspase-3 of the M group increased (
P
<
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(
P
<
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 (
P
<
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
2
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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