Vascular protective effects of aqueous extracts of Tribulus terrestris on hypertensive endothelial injury.
10.1016/S1875-5364(17)30088-2
- Author:
Yue-Hua JIANG
1
;
Jin-Hao GUO
2
;
Sai WU
3
;
Chuan-Hua YANG
4
Author Information
1. Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250011, China.
2. Shandong University of Traditional Chinese Medicine, Jinan 250355, China.
3. Qingdao Hiser medical group, Qingdao 266034, China.
4. Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250011, China. Electronic address: yang_chuanhua@hotmail.com.
- Publication Type:Journal Article
- Keywords:
Endothelial protection;
Hypertension;
Tribulus Terrestris
- MeSH:
Angiotensin II;
metabolism;
Animals;
Antihypertensive Agents;
administration & dosage;
Apoptosis;
drug effects;
Blood Pressure;
drug effects;
Endothelium, Vascular;
drug effects;
metabolism;
Human Umbilical Vein Endothelial Cells;
drug effects;
Humans;
Hypertension;
drug therapy;
genetics;
metabolism;
physiopathology;
Male;
NF-kappa B;
genetics;
metabolism;
Nitric Oxide Synthase Type III;
genetics;
metabolism;
Oxidative Stress;
drug effects;
Plant Extracts;
administration & dosage;
Proto-Oncogene Proteins c-akt;
genetics;
metabolism;
Rats;
Rats, Inbred SHR;
Rats, Inbred WKY;
Reactive Oxygen Species;
metabolism;
Tribulus;
chemistry
- From:
Chinese Journal of Natural Medicines (English Ed.)
2017;15(8):606-614
- CountryChina
- Language:English
-
Abstract:
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·d) for 6 weeks, using valsartan (13.5 mg·kg·d) 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 × 10 mol·L 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, PI3Kα, Erk2, FAK, and NF-κB p65 and protein expression of Erk2, FAK, and NF-κB p65. In conclusion, TT demonstrated anti-hypertensive and endothelial protective effects by regulating Erk2, FAK and NF-κB p65.
