Abstract
Objective To investigate the impact of autophagy in rat alveolar epithelial cells CCL149 to endoplasmic reticulum stress. Methods Building green fluorescent protein (GFP)-microtubelesas sociated protein light chain 3 (LC3) eukaryotic expression vector, and this plasmid was imported into CCL149 cells by plasmid transfection technology. The stable expression cell lines were screened to further study. Observing the level of cell autophagy and degree of endoplasmic reticulum stress in the time of hypoxia-reoxygenation (H/R) 2 hours, 4 hours, 6 hours after giving the process of autophagy activation agent (rapamycin) and autophagy inhibitors 3-Methyladenine (3-M). Results 3-MA pretreatment led to decreased LC3 (t=6.317, P=0.024; t=8.583, P=0.013; t=6.341, P=0.026), Beclin-1 (t=4.658, P=0.039; t=7.120, P=0.022; t=10.320, P=0.000) and p62 (t=5.906, P=0.015; t=7.032, P=0.019; t=7.072, P=0.032), and increased binding immunoglobulin protein (BIP) (t=5.988, P=0.012; t=9.473, P=0.004; t=12.863, P=0.000), X-Box Binding Protein 1 (XBP-1) (t=4.285, P=0.043; t=9.563, P=0.008; t=10.531, P=0.000) and C/EBP homologus protein (CHOP) (t=5.477, P=0.031; t=8.373, P=0.016; t=8.954, P=0.025) following H/R treatment at 2, 4 and 6 h. On the contrary, LC3 (t=4.502, P=0.046; t=10.000, P=0.010; t=4.983, P=0.041), Beclin-1 (t=5.161, P=0.029; t=5.767, P=0.029; t=9.342, P=0.012) and p62 (t=6.687, P=0.026; t=7.084, P=0.016; t=9.767, P=0.000) were enhanced, and BIP (t=7.245, P=0.016; t=8.432, P=0.005; t=12.562, P=0.000), XBP-1 (t=6.255, P=0.022; t=8.450, P=0.029; t=8.365, P=0.035) and CHOP (t=7.048, P=0.014; t=11.566, P=0.000; t=10.144, P=0.000) were decreased by treated with rapamycin following H/R treatment at 2, 4 and 6 h. Conclusion In the early of hypoxia reoxygenation, the endoplasmic reticulum stress was decreased as the autophagy enhanced in alveolar epithelial cells of rats. Key words: Hypoxia-reoxygenation; Autophagy; Endoplasmic reticulum stress
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