The aim of the present study was to investigate the effects of Xin-Ji-Er-Kang (XJEK) on high salt-induced hypertensive mice. Mice with high-salt diet-induced hypertension were divided into four groups: Control (standard diet alone for 8 weeks), model (diet containing 8% NaCl for 8 weeks and intragastric administration of distilled water for the last 4 weeks), XJEK + high-salt-treated (diet containing 8% NaCl for 8 weeks and intragastric administration of XJEK for the last 4 weeks) and irbesartan + high-salt-treated (diet containing 8% NaCl for 8 weeks with intragastric administration of irbesartan for the last 4 weeks). The hemodynamic index and cardiac pathological changes in the hypertensive mice were then examined. An aortic ring apparatus was used to detect acetylcholine-dependent endothelium relaxation function. Colorimetric analysis was applied to determine serum nitric oxide (NO), superoxide dismutase activity and malondialdehyde content; ELISA was employed to measure brain natriuretic peptide, serum angiotensin II (Ang II), endothelin-1 content and aldosterone; and immunohistochemistry was used to detect the expression of endothelial nitric oxide synthase (eNOS), interleukin (IL)-1β, IL-10 and tumor necrosis factor (TNF)-α in cardiac tissues. XJEK improved the heart systolic and diastolic function, ameliorated hemodynamic parameters and cardiovascular remodeling indices, blunted the cardiac pathological changes and improved endothelial dysfunction (ED) via boosting eNOS activity, promoting NO bioavailability and decreasing serum Ang II content. Furthermore, treatment with XJEK inhibited the increase of IL-1β and TNF-α expression and the decrease of IL-10 expression in cardiac tissues, and ameliorated oxidative stress status. Therefore, XJEK exerted protective effects against high salt-induced hypertension and cardiovascular remodeling in mice via improving ED, restoring pro- and anti-inflammatory factor balance and decreasing oxidative stress.
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http://dx.doi.org/10.3892/etm.2018.7105 | DOI Listing |
PLoS One
December 2024
Division of Medical Biochemistry, Tohoku Medical and Pharmaceutical University, Sendai, Japan.
The vascular endothelium is vital for cardio-pulmonary homeostasis and, thus, plays a crucial role in preventing life-threatening lung diseases. The transcription factor GATA2 is essential for hematopoiesis and maintaining vascular integrity. Heterozygous mutations in GATA2 can lead to a primary immunodeficiency syndrome with pulmonary manifestations.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
December 2024
Department of Health, Nutrition, and Food Science, Florida State University, Tallahassee, FL, USA.
Regulation of myocardial mass is key for maintaining cardiovascular health. This review highlights the complex and regulatory relationship between mechanosignaling and myocardial mass, influenced by many internal and external factors including hemodynamic and microgravity, respectively. The heart is a dynamic organ constantly adapting to changes in workload (preload and afterload) and mechanical stress exerted on the myocardium, influencing both physiological adaptations and pathological remodeling.
View Article and Find Full Text PDFMol Biol Rep
December 2024
Department of Physiology, School of Medicine, Shahid Sadoughi University of Medical Sciences, Yazd, Iran.
Background: The role of 1,25-dihydroxyvitamin-D3 (VitD) and sirtuin-1 (SIRT1) in mitigating pathological cardiac remodeling is well recognized. However, the potential for SIRT1 to mediate the inhibitory effects of VitD on angiotensin II (Ang II) -induced hypertrophy in H9c2 cardiomyoblasts remains unclear.
Methods: H9c2 cardiomyoblasts were exposed to Ang II or a combination of VitD and Ang II, both in the absence and presence of SIRT1-specific siRNA.
Signal Transduct Target Ther
December 2024
Department of Cardiology, Angiology, Hemostaseology and Medical Intensive Care, Medical Faculty Mannheim, University Medical Centre Mannheim (UMM), Heidelberg University, 68167, Mannheim, Germany.
Mol Ther
December 2024
Centre for Cardiovascular Science, The Queen's Medical Research Institute, University of Edinburgh; Edinburgh EH16 4TJ, UK; CARIM school for cardiovascular sciences, Department of Pathology, Maastricht University Medical Center (MUMC); Maastricht 6229HX, The Netherlands. Electronic address:
Proliferation of vascular smooth muscle cells (vSMCs) is a crucial contributor to pathological vascular remodelling. MicroRNAs (miRNAs) are powerful gene regulators and attractive therapeutic agents. Here, we aim to systematically identify and characterise miRNAs with therapeutic potential in targeting vSMC proliferation.
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