Abstract
Background Xin-Ji-Er-Kang (XJEK) shows protective effects on the myocardial ischemic diseases in our previous reports. We hypothesized that XJEK may exert preventing effects on L-NAME induced hypertensive mice by ameliorating oxidative stress (OS) and endothelial dysfunction (ED). Methods After treatment with XJEK for four weeks, cardiac function and cardiovascular pathology changes were evaluated. Then, endothelial-dependent vascular relaxation and serum NO, eNOS, AMDA, SOD, MDA content, and cardiac tissue eNOS expression were detected. Results The hypertensive mice displayed distinct cardiovascular remodeling including increased HW/BW index (4.7 ± 0.33 versus 5.2 ± 0.34), cross-section area, and collagen deposition. In addition, ED was found manifested by decreased serum NO (20.54 ± 8.05 versus 6.29 ± 2.33), eNOS (28.34 ± 2.36 versus 20.37 ± 2.30), content, and decreased eNOS expression in cardiac tissue and damaged endothelium-dependent diastolic function. Moreover, OS was detected confirmed by decreased SOD activity and increased MDA content in serum. However, treatment with XJEK for 4 wk could reverse cardiovascular remodeling (HW/BW index normalized from 5.2 ± 0.34 to 4.59 ± 0.25), ameliorate and preserve endothelial function (NO: 16.67 ± 7.24 versus 6.29 ± 2.33; eNOS: 16.67 ± 7.24 versus 6.29 ± 2.33), and suppress OS. Conclusion XJEK has protective effects against cardiovascular remodeling in L-NAME induced hypertensive mice.
Highlights
Xin-Ji-Er-Kang (XJEK) shows protective effects on the myocardial ischemic diseases in our previous reports
Since reduced endothelial-dependent vasodilation was the main mechanism of L-NAMEinduced hypertension, we investigated the dilative response to acetylcholine (Ach) in aortic rings stimulated by phenylephrine compared to those in control group (P < 0.01, Figure 5)
Work by Furchgott and Zawadzki showed that the presence of endothelium was vital to acetylcholine induced vasorelaxation in isolated artery preparations and this effect was attributed to a substance(s) released by the endothelium [11], which was subsequently identified as nitric oxide (NO) [12], initially named endothelium derived relaxing factor (EDRF) [13, 14]
Summary
Xin-Ji-Er-Kang (XJEK) shows protective effects on the myocardial ischemic diseases in our previous reports. We hypothesized that XJEK may exert preventing effects on L-NAME induced hypertensive mice by ameliorating oxidative stress (OS) and endothelial dysfunction (ED). Endothelial-dependent vascular relaxation and serum NO, eNOS, AMDA, SOD, MDA content, and cardiac tissue eNOS expression were detected. Treatment with XJEK for 4 wk could reverse cardiovascular remodeling (HW/BW index normalized from 5.2 ± 0.34 to 4.59 ± 0.25), ameliorate and preserve endothelial function (NO: 16.67 ± 7.24 versus 6.29 ± 2.33; eNOS: 16.67 ± 7.24 versus 6.29 ± 2.33), and suppress OS. XJEK has protective effects against cardiovascular remodeling in L-NAME induced hypertensive mice. It has been confirmed that nitric oxide generated by endothelial isoform of nitric oxide synthase (eNOS) in the vascular endothelium plays a crucial part in the regulation of blood pressure. For the design of new options, it is crucial to have an in-depth understanding of the molecular mechanisms which regulate nitric oxide signaling under pathophysiological conditions [8]
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