Abstract
Samchulkunbi-tang (SCT, Shen Zhu Jian pi tang in Chinese) is said to have been first recorded by Zheng Zhi Zhun Sheng during the Ming Dynasty in China. Records of SCT in Korea are known to have been cited in Donguibogam (Dong Yi Bao Jian in Chinese), Uibang Hwaltu (Yi Fang Huo Tao in Chinese), and Bang Yak Hapyeon (Fang Yao He Bian in China). Although SCT is widely used in treating chronic gastritis and gastric ulcers, the beneficial effect on renal vascular function is unknown. Hypertension is a risk factor for cardiovascular disease and endothelial dysfunction in humans and experimental animal models of arterial hypertension. In addition, kidney dysfunction is characterized by hypertension diseases. This study was conducted to evaluate the effect of SCT on the vascular function in vitro (human umbilical cord endothelial cells, HUVECs) and in vivo (NG‐nitro‐L‐arginine methyl ester, L-NAME-induced hypertensive rats). The phosphorylation of protein kinase B (Akt) and endothelial nitric oxide synthase (eNOS) is closely related to nitric oxide (NO) production in HUVECs, and SCT in this study significantly increased these. For three weeks, hypertensive rat models were induced by L-NAME administration (40 mg/kg/day) with portable water. It was followed by oral administration with 100 and 200 mg/kg/day for two weeks to confirm the effectiveness of SCT. As a result, systolic blood pressure decreased in the SCT-treated groups, compared with that in the L-NAME-induced hypertensive group. SCT treatment restored vasorelaxation by stimulating acetylcholine and cGMP production in the thoracic aorta. In addition, SCT treatment decreased intima-media thickness, attenuated the reduction of eNOS expression, and increased endothelin-1 expression. It also increased p-Akt and p-eNOS expression in hypertensive rat aorta. Furthermore, regarding renal function parameters, SCT ameliorated urine osmolality, urine albumin level, serum creatinine, and blood urea nitrogen levels. These results demonstrate that the oriental medicine SCT exerts potent vascular and renal protective effects on nitric oxide-deficient hypertensive rats and HUVECs
Highlights
Hypertension, a representative disease of the cardiovascular system, is known to cause conditions such as cardiac hypertrophy and renal dysfunction, thereby reducing cardiovascular function [1]
Hypertension-induced renal dysfunction is characterized by persistent systemic blood pressure overload, which gradually exceedsIn hypertensive patients, it is known that there is a correlation with body fluids, which causes heart failure and kidney failure to coexist the autoregulatory mechanism to maintain an adequate glute filtration pressure [6]. erefore, Evidence-Based Complementary and Alternative Medicine glomerular hypertrophy and proteinuria induced by renal dysfunction are associated with persistent inflammation and cause circulatory dysfunction [7], which leads to endothelial dysfunction [8]
It promotes the action of soluble guanylyl cyclase, which promotes the conversion of guanosine 5′-triphosphate (GTP) to cyclic guanosine 3′,5′-monophosphate, and cGMP produced by nitric oxide (NO) causes smooth muscle relaxation
Summary
Hypertension, a representative disease of the cardiovascular system, is known to cause conditions such as cardiac hypertrophy and renal dysfunction, thereby reducing cardiovascular function [1]. It is known that there is a correlation with body fluids, which causes heart failure and kidney failure to coexist [4, 5]. Hypertension-induced renal dysfunction is characterized by persistent systemic blood pressure overload, which gradually exceedsIn hypertensive patients, it is known that there is a correlation with body fluids, which causes heart failure and kidney failure to coexist the autoregulatory mechanism to maintain an adequate glute filtration pressure [6]. E conversion of NO-arginine to citrulline produces NO catalyzed by NO synthase (NOS) It promotes the action of soluble guanylyl cyclase (sGC), which promotes the conversion of guanosine 5′-triphosphate (GTP) to cyclic guanosine 3′,5′-monophosphate (cGMP), and cGMP produced by NO causes smooth muscle relaxation. L-NAME causes blood vessel dysfunction and nephrotic blood vessel contraction
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