Abstract
BackgroundXinJiErKang (XJEK), a Chinese herbal formula, is identified as an effective preparation to treat coronary heart disease and myocarditis. The aim of the study is to investigate the anti-hypertensive effects of XJEK by oral administration and also to find out whether the drug has any role in oxidative stress and vascular endothelial function.MethodsClipping of the renal artery resulted in gradual elevation of the systolic blood pressure (SBP) which reached a plateau after 4 weeks of surgery. Treatment of hypertensive rats (20 mmHg higher than basic systolic blood pressure) with XJEK (6, 12, 24 g/kg/day) and fosinopril (15 mg/kg/day) respectively by intragastric administration started 4 weeks after surgery and continued for 4 weeks. The sham-operated (Sh-Op) controls received drinking water. BP was monitored weekly using tail-cuff apparatus. At the end of 8 wk, left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), rate of rise of left ventricular pressure (±dp/dtmax) were examined (PowerLab 8/30, AD Instruments, Australia). The myocardial hypertrophy index was expressed as heart weight/body weight (HW/BW), the histological changes were investigated by hematoxylin and eosin (HE) and Van Gieson (VG) stain. Endothelium-dependent relaxations due to acetylcholine were observed in isolated rat thoracic aortic ring preparation. Superoxide dismutase (SOD) activity, malondialdehyde (MDA) and nitric oxide (NO) content in serum, contents of hydroxyproline (Hyp) in the ventricular tissue were assayed by xanthin oxidase method, thiobarbituric acid (TBA) method, Griess method and alkaline hydrolysis method, respectively. Angiotensin II (Ang II) content in serum was detected by radioimmunoasssay method.ResultsXJEK therapy potently improved cardiac function, inhibited myocardial hypertrophy, improved cardiac pathology change, decreased the myocardial cross-section area (CSA), collagen volume fraction (CVF) and perivascular circumferential collagen area (PVCA), reduced the content of Hyp in the left ventricular tissue, inhibited the decrease of SOD activity and increase of MDA, Ang II content in serum. Moreover, treatment with XJEK improved endothelial dysfunction (ED) manifested by promoting endothelial-dependent vasodilation of thoracic aortic rings and enhancing the NO activity in serum.ConclusionsThese findings suggest that administration of XJEK possess protective effects against 2K1C induced hypertension and cardiac remodeling in rats, preserve NO activity and endothelial function.
Highlights
XinJiErKang (XJEK), a Chinese herbal formula, is identified as an effective preparation to treat coronary heart disease and myocarditis
Long-term hypertension often results in left ventricular hypertrophy, which is considered to be a risk factor for coronary heart disease, congestive heart failure (CHF), ventricular arrhythmia, and sudden death [1], as well as structural alteration of the vascular wall, which is manifested by endothelial dysfunction (ED), extracellular matrix deposition and medial layer thickening because of hypertrophy/hyperplasia and migration of vascular smooth muscle cells (VSMCs)
Effect of XJEK on systolic blood pressure (SBP) SBP was considerably lower in the XJEK and fosinopril treated hypertensive rats as compared to experimentally induced hypertensive model group
Summary
XinJiErKang (XJEK), a Chinese herbal formula, is identified as an effective preparation to treat coronary heart disease and myocarditis. The aim of the study is to investigate the anti-hypertensive effects of XJEK by oral administration and to find out whether the drug has any role in oxidative stress and vascular endothelial function. Hypertension is manifested by an increased arterial pressure, it involves the complex structural and functional alterations of its target organs. Long-term hypertension often results in left ventricular hypertrophy, which is considered to be a risk factor for coronary heart disease, congestive heart failure (CHF), ventricular arrhythmia, and sudden death [1], as well as structural alteration of the vascular wall, which is manifested by endothelial dysfunction (ED), extracellular matrix deposition and medial layer thickening because of hypertrophy/hyperplasia and migration of vascular smooth muscle cells (VSMCs). One of the key factors in ED is the overproduction of ROS which participates in the development of hypertension, atherosclerosis, diabetes, cardiac hypertrophy, heart failure, ischemia-reperfusion injury, and stroke [8]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
