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Virgin rice bran oil alleviates hypertension through the upregulation of eNOS and reduction of oxidative stress and inflammation in L-NAME–induced hypertensive rats

Jan-on, Gulladawan, Sangartit, Weerapon, Pakdeechote, Poungrat, Kukongviriyapan, Veerapol, Sattayasai, Jintana, Senaphan, Ketmanee, Kukongviriyapan, Upa
Nutrition 2020 v.69 pp. 110575
additive effect, animal disease models, antihypertensive effect, antioxidants, bioavailability, blood plasma, blood pressure, cholesteremic effect, diet, drug therapy, endothelial nitric oxide synthase, hypertension, inflammation, malondialdehyde, nitrates, nitric oxide, nitrites, nutrition risk assessment, oxidative stress, peptidyl-dipeptidase A, rats, rice bran oil, tissues, transcription factor NF-kappa B, tumor necrosis factor-alpha, vascular cell adhesion molecules
Endothelial dysfunction associated with reduction in nitric oxide (NO) bioavailability plays an important role in development of hypertension. Consumption of a diet rich in antioxidants appears to lower the risk for hypertension. Virgin rice bran oil (VRBO) possesses antioxidant, anti-inflammatory, and hypocholesterolemic activities. However, to our knowledge, the antihypertensive effect of VRBO has not been investigated. The aim of this study was to examine the antihypertensive effect of VRBO in Nω-nitro-l-arginine methyl ester (L-NAME)-induced hypertensive rats and its underlying mechanisms.Hypertension was induced in rats by administration of L-NAME, after which VRBO, lisinopril (Lis), or VRBO + Lis was administered. Studies were then conducted on the hemodynamics of vascular responses to vasoactive substances, plasma angiotensin-converting enzyme (ACE), plasma nitrate/nitrite, oxidative stress, and inflammatory markers.L-NAME administration induced hemodynamic changes including elevation of blood pressure, increased peripheral vascular resistance, and endothelial dysfunction. Reduction in plasma nitrate/nitrite, overproduction of vascular superoxide, and increases in plasma ACE, malondialdehyde, protein carbonyl, and plasma tumor necrosis factor-α were observed in L-NAME hypertensive rats. The changes were associated with a marked decrease in endothelial NO synthase expression, increased expression of gp91phoxand vascular cell adhesion molecule-1, and activation of nuclear factor-κB in aortic tissues. Administration of either VRBO or Lis significantly mitigated all of these deleterious effects. The combination of VRBO and Lis was more effective than either treatment alone.The antihypertensive effect of VRBO may be mediated by restoration of hemodynamics, increased NO bioavailability, and alleviation of oxidative stress and inflammation. VRBO has an additive effect on antihypertensive medication.