Moringa oleifera leaf extract enhances endothelial nitric oxide production leading to relaxation of resistance artery and lowering of arterial blood pressure.

A mass of evidence has identified a promoting of nitric oxide (NO) production in endothelial cells using natural products as a potential strategy to prevent and treat hypertension. This study investigated whether the aqueous extract of Moringa oleifera leaves (MOE) could lower mean arterial pressure (MAP) and relax mesenteric arterial beds in rats via stimulating endothelium-derived NO production. Intravenous administration of MOE (1-30 mg/kg) caused a dose-dependent reduction in MAP in anesthetized rats. In rats pretreated with the NO-synthase inhibitor, Nω-nitro-L-arginine methyl ester (L-NAME, 30 mg/kg, i.v.), the effect of MOE on MAP was significantly reduced. MOE (0.001-3 mg) induced relaxation in methoxamine (10 µM) pre-contracted mesenteric arterial beds, which was abolished by endothelium denudation. This endothelium-dependent vasorelaxation was reduced by L-NAME (100 µM) or the NO-sensitive guanylyl cyclase inhibitor, 1H- [1,2,4]-oxadiazolo-[4,3-a]-quinoxalin-1-one (10 µM). In primary human pulmonary artery endothelial cells, MOE (3-30 µg/mL) induced NO production, which was inhibited by L-NAME (100 µM) pretreatment. These findings show that MOE stimulates the endothelium-derived NO release for driving its vasorelaxation to lower arterial blood pressure. These suggest the development of MOE as a natural antihypertensive supplement.

Platelet inhibitory effects of juices from Pachyrhizus erosus L. root and Psidium guajava L. fruit: a randomized controlled trial in healthy volunteers.

BACKGROUND: The purpose of this study is to investigate cardiovascular benefits of juices obtained from two commonly consumed fruits in Thailand, Pachyrhizus erosus, L. (yam bean) and Psidium guajava, L. (guava), by examining their acute cardiovascular effects in healthy volunteers. Possible involvements of the dietary nitrate on their effects were investigated as well. METHOD: Thirty healthy volunteers were randomly divided into three groups of 10 subjects per group and each group was allocated to drink 500 ml of freshly prepared yam bean root juice, guava fruit juice, or water. Systemic nitrate and nitrite concentrations, heart rate, systolic and diastolic blood pressure, serum K(+) concentrations, ex vivo platelet aggregation, and plasma cGMP concentrations were monitored at the baseline and at various time points after the intake of juices or water. Data were compared by repeated measures ANOVA. RESULTS: Following the ingestion of both yam bean root juice and guava fruit juice, collagen-induced but not ADP-induced platelet aggregation was attenuated. Ingestion of yam bean root juice increased systemic nitrate and nitrite concentrations whereby elevated nitrite concentrations correlated with the extent of inhibiting collagen-induced platelet aggregation. In addition, positive correlation between systemic nitrite and plasma cGMP concentrations and negative correlation between plasma cGMP concentrations and the extent of collagen-induced platelet aggregation were revealed. Nevertheless, yam bean root juice reduced only diastolic blood pressure while guava fruit juice reduced heart rate, systolic and diastolic blood pressure. CONCLUSION: The present study has illustrated, for the first time, acute inhibitory effects of yam bean root juice and guava fruit juice on ex vivo collagen-induced platelet aggregation in healthy subjects. Dietary nitrate was shown to underlie the effect of yam bean root juice but not that of guava fruit juice. Following yam bean root juice ingestion, systemic nitrate apparently converts to nitrite and further to NO which may attenuate platelet responses to collagen stimulation. Cardiovascular benefits of juices from yam bean root and guava fruit are noteworthy in term of the cardiovascular health-promoting approach. TRIAL REGISTRATION: Randomized controlled trial TCTR20150228001 .

Improved WOMAC score following 16-week treatment with bromelain for knee osteoarthritis.

Treatment with bromelain-containing enzyme preparation for 3-4 weeks is effective for treatment of knee osteoarthritis (OA). Here, we aimed to assess 16-week treatment with bromelain in mild-to-moderate knee OA patients. We performed a randomized, single-blind, active-controlled pilot study. Forty knee OA patients were randomized to receive oral bromelain (500 mg/day) or diclofenac (100 mg/day). Primary outcome was the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) analyzed by Wilcoxon signed rank test. Secondary outcome was the short-form 36 (SF-36). Plasma malondialdehyde (MDA) and nitrite were measured as oxidative stress markers. There was no difference in WOMAC and SF-36 scores compared between bromelain and diclofenac groups after 4 weeks. At week 4, the improvement of total WOMAC and pain subscales from baseline was observed in both groups; however, two patients given diclofenac had adverse effects leading to discontinuation of diclofenac. However, observed treatment difference was inconclusive. At week 16 of bromelain treatment, the patients had improved total WOMAC scores (12.2 versus 25.5), pain subscales (2.4 versus 5.6), stiffness subscales (0.8 versus 2.0), and function subscales (9.1 versus 17.9), and physical component of SF-36 (73.3 versus 65.4) as compared with baseline values. OA patients had higher plasma MDA, nitrite, and prostaglandin E2 (PGE2) in lipopolysaccharide (LPS)-stimulated whole blood but lower plasma α-tocopherol than control subjects. Plasma MDA and LPS-stimulated PGE2 production were decreased at week 16 of bromelain treatment. Bromelain has no difference in reducing symptoms of mild-to-moderate knee OA after 4 weeks when compared with diclofenac.

Extracellular heme enhances the antimalarial activity of artemisinin.

Artemisinin exerts the antimalarial activity through activation by heme. The hemolysis in malaria results in the elevated levels of plasma heme which may affect the activity of artemisinin. We hypothesized that the extracellular heme would potentiate the antimalarial activity of artemisinin. Hemin (ferric heme) at the pathologic concentrations enhanced the activity of artemisinin against Plasmodium falciparum in vitro and increased the levels of the lipid peroxidation products in the presence of artemisinin. The antimalarial activity of artemisinin and potentiation by hemin was decreased by vitamin E. Hemin had no effect on the activity of quinoline drugs (chloroquine, quinine and mefloquine). Furthermore, the oxidative effect of hemin in the presence of artemisinin or quinoline drugs was studied using low-density lipoprotein (LDL) oxidation as a model. Artemisinin enhanced the effects of hemin on lipid peroxidation and a decrease of tryptophan fluorescence in LDL whereas the quinoline drugs inhibited the oxidation by hemin. In conclusion, the extracellular hemin enhances the antimalarial activity of artemisinin as a result of the increasing oxidative effect of hemin.