Đang chuẩn bị nút TẢI XUỐNG, xin hãy chờ
Tải xuống
Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học 'Respiratory Research cung cấp cho các bạn kiến thức về ngành y đề tài:"Role of chymase in cigarette smoke-induced pulmonary artery remodeling and pulmonary hypertension in hamsters. | Wang et al. Respiratory Research 2010 11 36 http respiratory-research.eom content 11 1 36 RESPIRATORY RESEARCH RESEARCH Open Access Role of chymase in cigarette smoke-induced pulmonary artery remodeling and pulmonary hypertension in hamsters 1t 1.2t 3 1 1 1 1 P s Tao Wang Su-Xia Han Shang-Fu Zhang Yun-Ye Ning Lei Chen Ya-Juan Chen Guang-Ming He Dan Xu Jin An 1 Ting Yang1 Xiao-Hong Zhang1 Fu-Qiang Wen1 Abstract Background Cigarette smoking is an important risk factor for pulmonary arterial hypertension PAH in chronic obstructive pulmonary disease COPD . Chymase has been shown to function in the enzymatic production of angiotensin II AngII and the activation of transforming growth factor TGF -p1 in the cardiovascular system. The aim of this study was to determine the potential role of chymase in cigarette smoke-induced pulmonary artery remodeling and PAH. Methods Hamsters were exposed to cigarette smoke after 4 months lung morphology and tissue biochemical changes were examined using immunohistochemistry Western blotting radioimmunoassay and reversetranscription polymerase chain reaction. Results Our results show that chronic cigarette smoke exposure significantly induced elevation of right ventricular systolic pressures RVSP and medial hypertrophy of pulmonary arterioles in hamsters concurrent with an increase of chymase activity and synthesis in the lung. Elevated Ang II levels and enhanced TGF-p1 Smad signaling activation were also observed in smoke-exposed lungs. Chymase inhibition with chymostatin reduced the cigarette smoke-induced increase in chymase activity and Ang II concentration in the lung and attenuated the RVSP elevation and the remodeling of pulmonary arterioles. Chymostatin did not affect angiotensin converting enzyme ACE activity in hamster lungs. Conclusions These results suggest that chronic cigarette smoke exposure can increase chymase activity and expression in hamster lungs. The capability of activated chymase to induce Ang II formation and .
