The Expression And Correlation Analysis Of PERK And EIF2α Protein In Rat Model Of COPD

Objective:To study effects of the activation of PERK and eIF2a protein in the apoptosis of pulmonary tissue in COPD rate model, by comparing the differentiation and correlation during PERK, eIF2a and CHOP.Methods:24Wister male rates were randomly divided in to2groups:Control group and COPD model group. COPD model group were exposed to cigarette smoke for2nd-13th,15th-30th day every morning and intratracheal injection with lipopolysaccharide(LPS) on the1st and14th day. Control group were not exposed to cigarette somke and intratracheal injection with normal saline instead. Calculate FEV0.3/FVC, RI and Cdyn by computer process. Kill the mouse by femoral artery bloodletting, and keep the lung tissues in4%paraformaldehyde and liquid nitrogen. Make Pathological morphology. The apoptosis level of the lung tissue was analyzed by TUNEL. The expression of p-PERK,p-eIF2α,CHOP in lung tissues were examined using immunohistochemistry and Western blot. Student's t test and Pearson correlation coefficient were used for data analysis.Results:(1) Compared to the control group, there is a significant decline in their lung funtion than the normal ones, with falling in FEV0.3/FVC and Cydn and rising in RI.These differences were statistically significant (P<0.05), indicating that there was the airflow limitation and obstructive pulmonary dysfunction, and increased-resistance in the small airway.(2) The pathology of the model rats' lung tissues was characterized by chronic bronchitis and pulmonary emphysema.(3) The apoptosis rate of the lung tissue was obviously difference between the control group and the COPD model group (P<0.05). AI of the model rats was almost41%higher than the control ones.(4) The results of immunohistochemistry and Western blot showed that expression levels of apoptosis-related protein CHOP was also higher in the model group. The expression of activated signal molecules p-PERK and p-eIF2α in model rats' lungs elevated markedly compared with that in normal ones. These differences were statistically significant (P<0.05).(5) Correlation analysis:in COPD model group, the expression levels of p-PERK,p-eIF2a are positive correlation with CHOP protein(r=0.790, r=0.643).Conclusions:(1) COPD Rat models were successfully established through smoking and intratracheal instillation of lipopolysaccharide (LPS).(2) The activation of PERK and eIF2a pay an role in the occurrence of pulmonary tissue apoptosis in COPD rat model.