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Vascular protective effects of aqueous extracts of Tribulus terrestris on hypertensive endothelial injury

机译:Tribulus Terrestris水提取物对高血压内皮损伤的血管保护作用

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Angiotensin II (Ang II) is involved in endothelium injury during the development of hypertension. Tribulus terrestris (TT) is used to treat hypertension, arteriosclerosis, and post-stroke syndrome in China. The present study aimed to determine the effects of aqueous TT extracts on endothelial injury in spontaneously hypertensive rats (SHRs) and its protective effects against Ang II-induced injury in human umbilical vein endothelial cells (HUVECs). SHRs were administered intragastrically with TT (17.2 or 8.6 g.kg(-1).d(-1)) for 6 weeks, using valsartan (13.5 mg.kg(-1).d(-1)) as positive control. Blood pressure, heart rate, endothelial morphology of the thoracic aorta, serum levels of Ang II, endothelin-1 (ET-1), superoxide dismutase (SOD) and malonaldehyde (MDA) were measured. The endothelial injury of HUVECs was induced by 2 x 10(-6) mol.L-1 Ang II. Cell Apoptosisapoptosis, intracellular reactive oxygen species (ROS) was assessed. Endothelial nitric oxide synthase (eNOS), ET-1, SOD, and MDA in the cell culture supernatant and cell migration were assayed. The expression of hypertension-linked genes and proteins were analyzed. TT decreased systolic pressure, diastolic pressure, mean arterial pressure and heart rate, improved endothelial integrity of thoracic aorta, and decreased serum leptin, Ang II, ET-1, NPY, and Hcy, while increased NO in SHRs. TT suppressed Ang II-induced HUVEC proliferation and apoptosis and prolonged the survival, and increased cell migration. TT regulated the ROS, and decreased mRNA expression of Akt1, JAK2, PI3K alpha, Erk2, FAK, and NF-kappa B p65 and protein expression of Erk2, FAK, and NF-kappa B p65. In conclusion, TT demonstrated antihypertensive and endothelial protective effects by regulating Erk2, FAK and NF-kappa B p65.
机译:血管紧张素II(Ang II)在高血压发育过程中涉及内皮损伤。 Tribulus Terrestris(TT)用于治疗中国的高血压,动脉硬化和中风后综合征。本研究旨在确定TT提取物水溶液对自发性高血压大鼠(SHR)内皮损伤的影响及其对人脐静脉内皮细胞(HUVECS)的抗ang II诱导损伤的保护作用。使用Valsartan(13.5mg.kg(-1).D(-1))作为阳性对照,用TT(17.2或8.6g.kg(-1))造成TT(17.2或8.6g.kg(-1).d(-1)),用TT(17.2或8.6g.kg(-1))给药6周。测量胸主动脉血压,心率,内皮形态,测量血清Ang II,内皮蛋白-1(ET-1),超氧化物歧化酶(SOD)和苯甲醛(MDA)的血清水平。 Huvecs的内皮损伤诱导2×10( - 6)摩尔.L-1 Ang II。评估细胞凋亡,细胞内反应性氧物质(ROS)。测定细胞培养上清液和细胞迁移中的内皮一氧化氮合酶(ENOS),ET-1,SOD和MDA。分析了高血压连接基因和蛋白质的表达。 TT降低了收缩压,舒张压,平均动脉压和心率,改善了胸主动脉的内皮完整性,并降低了血清瘦素,Ang II,ET-1,NPY和Hcy,而在SHR中增加。 TT抑制了Ang II-诱导的Huvec增殖和凋亡,延长了生存率,并增加了细胞迁移。 TT调节ROS,降低AKT1,JAK2,PI3Kα,ERK2,FAK和NF-Kappa B P65和ERK2,FAK和NF-Kappa B P65的蛋白表达的MRNA表达。总之,TT通过调节ERK2,FAK和NF-Kappa B P65来表现出抗高血压和内皮保护作用。

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