Xiaodong Yang1, Chenxu Zhao1, Xuemei Ma1, Shanzuan Wang2, *
1Department of Respiratory and Critical Care Medicine, the First Affiliated Hospital of Jiamusi University, Jiamusi 154002, PR China - 2Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Putian University, Putian 351100, PR China
Objective: The purpose of this study is to reveal that endoplasmic reticulum stress is induced by alveolar epithelial cells of rats with chronic obstructive pulmonary disease (COPD), and that endoplasmic reticulum stress in COPD may be an important way to mediate the apoptosis of alveolar epithelial cells.
Methods: This study set up four experimental objects: COPD group, endoplasmic reticulum group, blank control group, and GRP78 group. Through the establishment of a COPD rat model, the endoplasmic reticulum stress markers GRP78, COPD, apoptosis morphology, and activated caspase-3 protein water were detected. Then, the lung function of rats was detected by H&E staining, and the levels of SOD and MDA in plasma were measured.
Results: The results indicate that the amount of SOD in endoplasmic reticulum stress-induced COPD was 15.30±0.62 u/ml, which was close to 10 u/ml. Compared with the blank control group, the content of the COPD group also decreased and the value range was 21.47±1.52 u/ml. Finally, there were 48 apoptotic cells in the endoplasmic reticulum group, followed by 38 in the COPD group and 33 in the blank control group.
Conclusion: Endoplasmic reticulum stimulation induces apoptosis of alveolar epithelial cells in rats with COPD and the anti-apoptotic effect of GRP78.
Endoplasmic reticulum, alveolar epithelial cells, apoptosis rate, glucose regulatory proteins.