To examine the effects of houttuynin on ventricular remodeling induced by coronary artery ligation in rats and the underlying mechanisms. A rat model of ventricular remodeling was established by left coronary artery ligation (CAL). Rats were randomly divided into four groups: CAL control, CAL plus 40 mg/kg captopril, CAL plus 100 mg/kg houttuynin and sham-operated control. The rats were administered intragastrically with the corresponding drugs or distilled water for 7 weeks. At the end of the experiment, the left ventricular weight index (LVWI) and heart weight index (HWI) were determined. Myocardium tissue was stained with hematoxylin and eosin or picric acid/Sirius red for cardiomyocyte cross-section area or collagen content measurements respectively. The concentrations of angiotensin I (Ang I), angiotensin II (Ang II), aldosterone (ALD) and endothelin-1 (ET-1) in myocardium or serum were detected by radioimmunoassay. The hydroxyproline (Hyp) concentration was measured by alkali hydrolysis. Ultraviolet spectrophotometry was used to determine glutathione peroxidase (GSH-Px) and catalase (CAT) activities in serum. Houttuynin significantly diminished LVWI and HWI, decreased Ang I, Ang II, ALD, ET-1 and Hyp concentrations in myocardium or serum, increased NO concentration and GSH-Px, CAT activities after 7 weeks of treatment. Houttuynin could also reduce cardiomyocyte cross-section area and collagen deposition. Houttuynin attenuates ventricular remodeling in coronary artery ligation rats by restricting the excessive activation of rennin-angiotensin-aldosterone system (RAAS) and the peroxidation.
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http://dx.doi.org/10.1016/j.ejphar.2014.07.015 | DOI Listing |
Sci Rep
January 2025
General Hospital of Xinjiang Military Command, 359 North Friendship Road, Sayibak, Ürümqi, 830000, Xinjiang, China.
The inflammatory response of lung tissue and abnormal proliferation of pulmonary artery smooth muscle cells are involved in the pathogenesis of high-altitude pulmonary hypertension (HAPH). Halofuginone (HF), an active ingredient derivative of Chang Shan (Dichroa febrifuga Lour. [Hydrangeaceae]), has antiproliferative, antihypertrophic, antifibrotic, and other effects, but its protective effects on HAPH remains unclear.
View Article and Find Full Text PDFAnn Thorac Cardiovasc Surg
January 2025
Division of Thoracic Surgery, Department of Surgery, Kobe University Hospital and Graduate School of Medicine, Kobe, Hyogo, Japan.
Purpose: The underlying mechanism why segmentectomy has demonstrated the non-inferiority to lobectomy in several randomized trials remains unclear. Computed tomography (CT)-measured pulmonary artery (PA) enlargement reflects PA pressure and predicts the prognosis of certain respiratory diseases. We compared the preoperative and postoperative PA diameter to the ascending aorta diameter (PA/A) ratio, investigating its impact on right ventricular function in lung resection.
View Article and Find Full Text PDFJ Vis Exp
January 2025
Mechanical, Aerospace, and Biomedical Engineering, University of Tennessee;
Cardiovascular disease (CVD) is the leading cause of death in the United States. Damage in the cardiovascular system can be due to environmental exposure, trauma, drug toxicity, or numerous other factors. As a result, cardiac tissue and vasculature undergo structural changes and display diminished function.
View Article and Find Full Text PDFCirc Cardiovasc Imaging
January 2025
Multimodality Cardiac Imaging Section, IRCCS Policlinico San Donato, Milan, Italy (L.T., G.D., M.L., A.C.).
Echocardiography
February 2025
Department of Cardiology, Loyola University Medical Center, Maywood, Illinois, USA.
The left atrium (LA) is pivotal in cardiac hemodynamics, serving as a dynamic indicator of left ventricular (LV) compliance and diastolic function. The LA undergoes structural and functional adaptations in response to hemodynamic stress, infiltrative processes, myocardial injury, and arrhythmic triggers. Remodeling of the LA in response to these stressors directly impacts pulmonary circulation, eventually leading to pulmonary capillary involvement, pulmonary artery hypertension, and eventually right ventricular failure.
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