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Anti-atherogenic effects of the methanol extract of Sorbus cortex in atherogenic-diet rats.

机译:花or皮甲醇提取物对动脉粥样硬化饮食大鼠的抗动脉粥样硬化作用。

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The present study was designed to examine whether the methanol extract of Sorbus commixta cortex (MSC) could prevent the development of atherosclerosis through regulating the vascular nitric oxide (NO) and endothelin-1 (ET-1) systems in atherogenic-diet rats. Our findings show that aortic NO production as well as endothelial nitric oxide synthase (ecNOS) expression was significantly decreased in atherogenic-diet rats compared with those in the control group. Aortic ET-1 expression was augmented in rats fed an atherogenic-diet while NF-kappaB p65 was upregulated. Treatment of atherogenic-diet rats with either low (100 mg/kg/d) or high (200 mg/kg/d) doses of MSC led not only to significant increases in the aortic NOS/NO system, but also to decreases in aortic ET-1 expression. The aortic expression level of NF-kappaB p65 was also attenuated in atherogenic-diet rats by chronic treatment with low or high doses of MSC. Atherogenic-diet induced increases in the expression of adhesion molecules including intercellular adhesion molecules-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and E-selectin were markedly decreased by treatment with MSC. From the histopathological examination, MSC treatment was shown to lessen the thickening noted in the aortic intima and media of the atherogenic-diet rats. These results suggest that MSC affects the atherogenic process via the suppression of proinflammatory and adhesion molecules in atherogenic-diet rats, which may be, at least in part, causally related with the regulation of vasoactive systems such as the NO and ET-1 systems.
机译:本研究的目的是通过调节动脉粥样硬化饮食大鼠中的血管一氧化氮(NO)和内皮素-1(ET-1)系统来检查花or(MSC)的甲醇提取物是否可以预防动脉粥样硬化的发展。我们的研究结果表明,与对照组相比,在致动脉粥样化饮食的大鼠中,主动脉NO的产生以及内皮型一氧化氮合酶(ecNOS)的表达明显降低。动脉粥样化饮食的大鼠主动脉ET-1表达增加,而NF-κBp65上调。用低剂量(100 mg / kg / d)或高剂量(200 mg / kg / d)MSC治疗动脉粥样硬化饮食大鼠不仅导致主动脉NOS / NO系统显着增加,而且导致主动脉NOS / NO系统减少ET-1表达。通过低剂量或高剂量MSC的长期治疗,在动脉粥样硬化饮食大鼠中NF-κBp65的主动脉表达水平也减弱。 MSC处理显着降低了致热饮食引起的粘附分子表达的增加,包括细胞间粘附分子-1(ICAM-1),血管细胞粘附分子-1(VCAM-1)和E-选择素。从组织病理学检查来看,MSC治疗可减轻动脉粥样硬化饮食大鼠的主动脉内膜和中膜的增厚。这些结果表明,MSC通过抑制动脉粥样化饮食大鼠中的促炎和粘附分子来影响动脉粥样化过程,这可能至少部分与血管活性系统(如NO和ET-1系统)的调节有因果关系。

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