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Antagonistic Effect of All-trans Retinoic Acid against Dexamethasone on Apoptosis of Human Airway Epithelial Cells 16HBE

Wang Yunting¹, Hu Jie¹, Zou Wenjing¹, Ding Fengxia^1,2, Tian Daiyin^1,2, Ying Linyan^1,2, Dai Jihong^1,2, Luo Zhengxiu^1,2, Fu Zhou^1,2, Niu Chao^1,2*

(¹Ministry of Education Key Laboratory of Child Development and Disorders, China International Science and Technology Cooperation base of Child development, Chongqing Key Laboratory of Pediatrics, Children’s Hospital of Chongqing Medical University, Chongqing 400014, China; ²Department of Respiratory Medicine Children’s Hospital of Chongqing Medical University, Chongqing 400014, China)

Abstract:

This paper will investigate the antagonistic effects of all-trans retinoic acid (ATRA) on the glucocorticoid-induced apoptosis of human airway epithelial cells. Human bronchial epithelial 16HBE cells were used as the research object, and treated with dexamethasone (Dex) at a concentration of 10 μmol/L and ATRA at a concentration of 1 μmol/L. 16HBE cells were cultured in vitro and divided into Control group, Dex group, ATRA group and Dex+ATRA group. The nuclear apoptosis of 16HBE cells was detected by TUNEL method. The membrane phosphatidylserine valgus was detected by Annexin V/PI double staining. The mitochondrial membrane potential was detected by fluorescent probe JC-1. The levels of apoptosis proteins Caspase-3 and Cleaved-caspase-3 were detected by Western blot. Compared with the Control group, more TUNEL-positive cells were observed in the Dex group, which significantly induced the up-regulation of Annexin V-positive protein, which led to a decrease in mitochondrial membrane potential and a significant increase in the levels of Caspase-3 and Cleaved-caspase-3. And ATRA can significantly suppress this trend caused by Dex. Dex can cause excessive apoptosis of human bronchial epithelial 16HBE cells, and ATRA can attenuate this effect of Dex.

CSTR: 32200.14.cjcb.2019.05.0014