Abstract
BackgroundIn the rat model of high carbohydrate, high fat (HCHF) diet-induced metabolic syndrome (MS), previous studies have found that asiatic acid has an antihypertensive effect. In this study, we investigated effects of asiatic acid on vascular structure, vascular function and renin-angiotensin system (RAS) in HCHF diet-induced MS rats.MethodsMale Sprague–Dawley rats were divided into three treatment groups for the 15 week study: a control group fed a normal diet, a MS group fed HCHF diet plus 15 % fructose in their drinking water for 15 weeks, and an asiatic acid treated group that received a HCHF diet plus fructose for 15 weeks and also received orally administered asiatic acid (20 mg/kg BW/day) for the final 3 weeks. Vascular structure and function were investigated. AT1 receptor expression in aortic tissues and eNOS protein expression in the mesenteric arteries were detected. The levels of serum angiotensin (Ang) II, angiotensin converting enzyme (ACE) and plasma norepinephrine (NE) were measured. The differences among treatment groups were analyzed by one-way analysis of variance (ANOVA) followed by post-hoc Bonferroni tests.ResultsAt the end of the study, all rats fed a HCHF diet exhibited signs of MS including, hypertension, dyslipidemia and insulin resistance. Vascular remodeling in large and small arteries, overexpression of AT1 receptor, and high levels of serum Ang II and ACE were also observed in MS group (p < 0.05). Contractile responses to sympathetic nerve stimulation were enhanced relating to high plasma NE level in MS rats (p < 0.05). The response to exogenous NE was not changed in the mesenteric bed. Vasorelaxation responses to acetylcholine were blunted in thoracic aorta and mesenteric beds, which is consistent with downregulation of eNOS expression in MS rats (p < 0.05). Restoration of metabolic alterations, hemodynamic changes, RAS and sympathetic overactivity, increased plasma NE, endothelium dysfunction, and downregulation of eNOS expression was observed in the asiatic acid treated group (p < 0.05). However, asiatic acid failed to alleviate vascular remodeling in MS rats.ConclusionOur findings suggest that the observed antihypertensive effect of asiatic acid in MS rats might be related to its ability to alleviate RAS overactivity and improve vascular function with restoration of sympathetic overactivity.Electronic supplementary materialThe online version of this article (doi:10.1186/s12906-016-1100-6) contains supplementary material, which is available to authorized users.
Highlights
In the rat model of high carbohydrate, high fat (HCHF) diet-induced metabolic syndrome (MS), previous studies have found that asiatic acid has an antihypertensive effect
Effects of asiatic acid on blood pressure and heart rate in conscious rats There were increases in Systolic blood pressure (SP) (145.6 ± 1.7 vs. 119.5 ± 1.9 mmHg) and HR (412.2 ± 4 vs. 361.6 ± 8.3 beat/min) in MS rats comparing to that levels in control rats (p < 0.01)
MS rats treated with asiatic acid for the last 3 weeks had a significant reduction of SP (128.5 ± 1.9 mmHg) and HR (382.2 ± 7.9 beat/min) when compared to those of untreated rats (p < 0.05; Fig. 1)
Summary
In the rat model of high carbohydrate, high fat (HCHF) diet-induced metabolic syndrome (MS), previous studies have found that asiatic acid has an antihypertensive effect. We investigated effects of asiatic acid on vascular structure, vascular function and renin-angiotensin system (RAS) in HCHF diet-induced MS rats. High carbohydrate-high fat (HCHF) diets have been shown to induce metabolic syndrome (MS) in rats. The development of hypertension in diet-induced MS in rats has been reported, along with structural and functional vascular alterations [4, 6]. Panchal and coworkers (2011) reported that HCHF diet-induced MS rats exhibited hypertension and a reduction of the vasorelaxation response to acetylcholine [8]. Microvascular dysfunction has been reported to be an important factor that contribute to the development of hypertension in MS rats [9]. Several mechanisms have been proposed in the pathogenesis of endothelial dysfunction, such as decrease in nitric oxide (NO) bioavailability and increases in oxidative stress and inflammation [10, 11]
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