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Updated: Dec 12, 2025
Oxygen-Glucose Deprivation and Reoxygenation as an In Vitro Ischemia-Reperfusion Injury Model for Studying Blood-Brain Barrier Dysfunction
Published on: May 7, 2015
Endoplasmic reticulum stress mediates osteocyte death under oxygen-glucose deprivation in vitro
Yizhong Wang1, Bing Han2, Junhui Ding2
1Department of Orthopaedics, Xiangyang No.1 People' Hospital, Hubei University of Medicine, Xiangyang, 441000, China; Department of Orthopedic Surgery, Zhongnan Hospital of Wuhan University, Wuhan, 430071, China.
Abstract:
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.
