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Effect of Naringin on Hypertension



Naringin supplementation was found to improve hypertension in high-carbohydrate/high-fat-diet–fed obese rats  and stroke-prone hypertensive rats. Moreover, naringin significantly increased the production of NO metabolites in urine and improved the acetylcholine-mediated endothelium function using thoracic aortic ring preparations by NO production. A similar vasodilatation effect was also observed in high-carbohydrate/high-fat-diet–fed obese rats and streptozotocin-induced diabetic rats . Calcium-dependent K channels are important regulators of vascular relaxation. Naringenin activated large conductance Ca2+-activated K+ currents in a concentration-dependent manner in rat tail artery myocytes.

The proliferation and migration of vascular smooth muscle cells (VSMCs) are critical events in the pathogenesis of atherosclerosis and hypertension. Naringenin inhibited TNF-α–induced VSMC proliferation and migration in a dose-dependent manner . It also blocked the increased reactive oxygen species (ROS) generation induced by TNF-α. Oxidative stress and TNF-α may also trigger the activation of mitogen-activated protein kinases (MAPKs), which are the key regulatory factors for VSMC proliferation. Naringenin prevented extracellular signal–regulated kinase (ERK)/MAPK and Akt phosphorylation, whereas p38 MAPK and c-Jun N-terminal kinases (JNKs) were unchanged. This overall effect is probably mediated via the induction of heme oxygenase 1 (HO-1) and reduction in oxidative stress.

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