Affiliations: Tasly Microcirculation Research Center, Peking University Health Science Center, Beijing, China | Tianjin University of Traditional Chinese Medicine, Tianjin, China | Department of Integration of Chinese and Western Medicine, School of Basic Medical Sciences, Peking University, Beijing, China
Note: [] Corresponding author: Jing-Yan Han, MD, PhD, Professor and Chairman, Department of Integration of Chinese and Western Medicine, School of Basic Medical Sciences, Peking University, 38 Xueyuan Road, Beijing 100191, People's Republic of China. Tel.: +86 10 8280 2862; Fax: +86 10 8280 2996; E-mail: [email protected]
Abstract: QiShen YiQi Pills® (QSYQ) is a compound Chinese medicine used for treatment of cardiovascular diseases. However, the potential of QSYQ to inhibit cardiac fibrosis in left ventricle hypertrophy is not explored to date. We investigated the effects of post-treatment with QSYQ on rat myocardial fibrosis in left ventricle hypertrophy induced by pressure over-load through ascending aortic stenosis. QSYQ was administrated 4 weeks after the surgery, at a dose of 0.8 g/kg/day over the next 4 weeks, while echocardiography was performed 4 and 8 weeks, respectively, after the surgery. Eight weeks after the surgery, myocardial blood flow was determined by Laser-Doppler Perfusion Imager and the ratio of heart weight to body weight (HW/BW) was estimated, in concurrent evaluation of myocardial histology and ultrastructure, as well as collagen content by sirius red staining, and immunohistochemistry staining for CD68 and transforming growth factor beta 1. Post-treatment with QSYQ significantly alleviated left ventricular posterior wall end diastolic thickness and the HW/BW, increased left ventricle ejection fraction and left ventricle fractional shortening. QSYQ also decreased myocardial fibrosis size. The expression of CD68 and transforming growth factor beta 1 were obviously suppressed after QSYQ treatment. The results suggest that post-treatment with QSYQ attenuates pressure over-load-induced cardiac hypertrophy and myocardial fibrosis through interfering in inflammatory process.
