Abstract
The Vitis labrusca is a grapevine that has antioxidant, neuroprotective, hepatoprotective, and anticarcinogenic activity. However, the effect of Vitis labrusca leaves on the cardiovascular system is yet to be ascertained. The present study was designed to investigate the effects of Vitis labrusca leaves extract (HP1) on cardiovascular remodeling in spontaneously hypertensive rats. Experiments were performed in rats and were randomly divided into the following groups: Wistar Kyoto rat (WKY), normal control group; spontaneously hypertensive rats (SHR), negative control group; SHR + Losa, positive control group (losartan, 10 mg/kg/daily, AT1 receptor blocker) and SHR + HP1 (100 mg/kg/daily). HP1 was orally administered daily for 4 weeks. The HP1 treatment significantly improved blood pressure, electrocardiographic parameters, and echocardiogram parameters compared to hypertensive rats. Additionally, the left ventricular (LV) remodeling and LV dysfunction were significantly improved in HP1-treated hypertensive rats. Furthermore, an increase in fibrotic area has been observed in hypertensive rats compared with WKY. However, administration of HP1 significantly attenuated cardiac fibrosis in hypertensive rats. Moreover, HP1 suppressed the expression of high mobility group box 1 (HMGB1), toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB), tumor necrosis factor alpha (TNF-α), interleukin-6 (IL-6), receptor for advanced glycation end products (RAGE), and extracellular signal-regulated kinases (ERK1/2) induced by hypertensive rats, resulting in improved vascular remodeling. Therefore, these results suggest that HP1 can improve the cardiovascular remodeling in hypertensive rats, and the mechanisms may be related to the suppressive effect of HP1 on HMGB1-TLR4-NFκB signaling in the cardiovascular system. Thus, the protective role of the traditional herbal medicine HP1 may provide new insights into the development of therapeutic drugs on the development of hypertensive cardiovascular dysfunction.
Highlights
Hypertension-related death is a major cause in modern society and is often associated with cardiovascular damage
receptor for advanced glycation end products (RAGE), and ERK1/2 expression was significantly decreased in HP1-treated rats 10 of compared with hypertensive rats (Figure 6B,C). These results showed that HP1 could improve vascular remodeling in the hypertensive rats by attenuating the high mobility group box 1 (HMGB1)-toll-like receptor 4 (TLR4)-NFκB signaling
We found that cardiac fibrosis is induced in the thoracic aorta of hypertensive rats compared to the Wistar Kyoto rat (WKY)
Summary
Hypertension-related death is a major cause in modern society and is often associated with cardiovascular damage. Hypertension with left ventricular (LV) hypertrophy and heart failure is a major independent risk factor for cardiovascular-related exchange rates and mortality in the aging population [1]. LV hypertrophy is a pathological change that causes myocardial fibrosis due to increased collagen content, which causes heart failure [3]. Damage to the barrier function of endothelial cells further increases the inflammatory response [11] that causes cardiovascular dysfunction [12]. It suggests that the inflammatory mechanism is an important participant in the pathology of hypertension. For the treatment of hypertension, long-term use of anti-hypertensive medication to treat high blood pressure can cause serious drug-resistance or side-effects. Natural substances used in traditional medicine are of interest in drug development because they have fewer side effects
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