As a vascularized organ, bone is known to be susceptible to ischemia. Ischemic osteonecrosis or skeletal unloading lead to ischemia in bone microenvironment that causes osteocytes to suffer hypoxia and nutrition deprivation.

Objective

To explore the effects of Oxygen-glucose deprivation (OGD) on osteocytes and the potential mechanism.

Methods

OGD model was established in cultured MLO-Y4 cell. Cell damage, intracellular oxidative stress and cell apoptosis were detected at different OGD times (0, 2, 4, 8, 12, 24 h), and the changes in endoplasmic reticulum (ER) stress-related indicators were observed. Furthermore, cells were treated with 4-phenylbutyrate sodium (4-PBA) to inhibit ER stress, and cell damage and oxidative stress level were detected.

Results

The cell viability under OGD exhibited a significantly reduced in a time-dependent manner, and the level of intracellular reactive oxygen species (ROS) were increased, cell apoptosis and ER stress was induced. Inhibition of ER stress can reduce cell death and intracellular ROS levels.

Conclusion

Our study demonstrated that ER stress regulates OGD-induced apoptotic cell death in MLO-Y4 cells via intracellular ROS.

中文翻译：

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内质网应激在体外氧葡萄糖剥夺下介导骨细胞死亡。

作为有血管的器官，骨骼容易受到局部缺血的影响。缺血性骨坏死或骨骼负荷导致骨骼微环境缺血，导致骨细胞缺氧和营养缺乏。

目的

探讨氧葡萄糖剥夺（OGD）对骨细胞的影响及其潜在机制。

方法

在培养的MLO-Y4细胞中建立OGD模型。在不同的OGD时间（0、2、4、8、12、24 h）检测到细胞损伤，细胞内氧化应激和细胞凋亡，并观察到内质网应激相关指标的变化。此外，用4-苯基丁酸钠（4-PBA）处理细胞以抑制ER应激，并检测了细胞损伤和氧化应激水平。

结果

OGD诱导的细胞活力呈时间依赖性显着降低，细胞内活性氧（ROS）水平升高，诱导细胞凋亡和内质网应激。抑制内质网应激可以减少细胞死亡和细胞内ROS水平。

结论

我们的研究表明，ER应激通过细胞内ROS调节OGD诱导的MLO-Y4细胞凋亡。