Endoplasmic Reticulum Stress-mediated Apoptosis In COPD Rat Model Of Aging State

Objective To observe cigarette smoke induced endoplasmic reticulum stress-apoptosis of alveolar epithelial cells in the COPD lung tissue of aging rats and CS induced endoplasmic reticulum stress on changes of aging.Methods Healthy male SD rats including24aged rats, age18months, weight (700±50) g;24adult rats age for3months, weight (300±20) g.48SD rats were randomly divided into four groups:adult control group, adult COPD model group, agedcontrol group and aged COPD model group,n=12.Copy rat model of COPD by the method of passive smoking plus intratracheal instillation of lipopolysaccharide Upon completion of the modeling measured the lung function of the rats in each group; pathological changes of the lung tissue; Immunohistochemical detected of CHOP, Caspase-12and p21expression and distribution in bronchopulmonary tissue; Western Blot detected the expression of CHOP, Caspase-12and p21; The TUNEL assay bronchopulmonary organization epithelial cell apoptosis.Results Lung function shows,compared with the control group,FEV0.3/FVC and Cdyn of the model group decreased significantly, while the RI was significantly higher.Compared with the adult group,these indicators in the elderly group were more obvious.HE staining of lung tissue showed that the model group rat alveolar wall destruction, alveolar space to expand and a significant reduction in the number of alveoli. Immunohistochemistry and Western Blot showed, compared with the control group,the apoptosis index CHOP and Caspase-12and aging index p21protein levels in model group rats lung tissue was significantly higher.Compared with the adult group,these indicators in the elderly group were higher.Compared with the control group, AI index of alveolar epithelial cells in the model group was significantly higher.Compared with the adult group,AI index in the elderly group was higher.Conclusion (1)Succeed in copying rat model of COPD by the method of passive smoking plus intratracheal instillation of lipopolysaccharide.(2) Endoplasmic reticulum stress-specific apoptosis molecular CHOP and Caspase-12expression in lung tissue of the aged model rats increased significantly, implied that aging may exacerbate the endoplasmic reticulum stress response.(3) Compared with the control group,aging specific molecular of p21expression in model group was higher, implied that increased endoplasmic reticulum stress response induced by cigarette promote the aging of the lung.(4) Endoplasmic reticulum stress and aging can promotes each other,which participates in the pathogenesis of COPD.