AMPK 调控内质网应激抵抗 COPD 大鼠肺泡上皮细胞凋亡的实验研究.

Objective: To explore the effect and mechanism of AMPK on apoptosis of alveolar epithelial cells induced by endoplasmic reticulum stress in COPD rats. Methods: the rats were divided into three groups: control group, model group, AICAR intervention group, establishment of rat model of chronic obstructive pulmonary disease by smoking smoke inhalation and intratracheal instillation of lipopolysaccharide. The HE staining of rat lung tissue pathological observation, immunohistochemical detection of p-AMPK /AMPK, western blot the expression of Caspase-3, ORP 150,and CHOP. Apoptosis were detected by TUNEL method. Results: the HE staining showed that the model group of pulmonary bullae formation, inflammatory cell infiltration, inflammatory ceils in AICAR group was lower than that of model group. Compared with the normal control group, immunohistochemistry and Western blot showed that p-AMPK/AMPK and ORP150 protein expression decreased in the model group,the difference was statistically significant (P＜0.05), and AICAR in the intervention group p-AMPK/AMPK and ORP150 protein expression were significantly increased compared with the model group,the difference was statistically significant (P＜0.05). Endoplasmic reticulum stress related apoptosis The expression of CHOP and caspase-3 apoptosis index increased significantly in the model group, there was significant difference compared with normal group (P＜0.05), while in group AICAR, apoptosis index down significantly compared with the model group. Conclusion: AMPK can protect alveolar epithelial cells from cigarette smoke induced endoplasmic reticulum stress and apoptosis, it was possible to achieve its protective effect the increase of ORP150. [ABSTRACT FROM AUTHOR]