关键词: 烟熏, 泛素特异性蛋白酶-19(USP-19), 慢性阻塞性肺疾病(COPD), 骨骼肌萎缩, 丝裂原活化蛋白激酶(MAPKs)

Abstract: Objective To investigate the effects of ubiquitin-specific peptidase 19 (USP-19) on rats bearing chronic obstructive pulmonary disease (COPD) induced by cigarette smoke (CS) exposure. Methods Rats exposed to chronic CS was chosen for the study. For histological examination, lungs and quadriceps femoris muscle were stained with hematozylin and eosin. Total RNA and protein were extracted for Real-time PCR and Western blot analysis to assess the MHC, USP-19 and MAPKs gene expression. Results Twelve weeks CS exposure produced lung lesions that morphologically resembled human emphysema, leading to the enlargement of alveolar ducts. Skeletal cell numbers per high-power (HP) lens increased after 12 weeks by 40% in comparison with the control group, suggesting muscle wasting. Chronic CS exposure decreased the mRNA level of MHC. MHC protein content in the quadriceps femoris muscle was decreased in the 8- and 12-week groups. CS significantly stimulated phosphorylation of ERK1/2, p38 without altering the total ERK1/2, p38 content. Conclusions Cigarette smoke-induced skeletal muscle atrophy is associated with up-regulation of USP-19, which via MAPKs probably.

Key words: Cigarette smoke exposure, Ubiquitin-specific peptidase 19 (USP-19), Chronic obstructive pulmonary disease (COPD), Muscle atrophy, Mitogen-activated protein kinases (MAPKs)