Background: Ethnopharmacological studies demonstrated the potential for Eulophia species to treat inflammation, cancer, and cardio-metabolic diseases. The aim of the study was to investigate the vasorelaxant effect of ethanolic Eulophia macrobulbon (EM) extract and its main phenanthrene on rat isolated mesenteric artery and to investigate the hypotensive effect of EM.Methods: The vasorelaxant effects of EM extract or phenanthrene and the underlying mechanisms were evaluated on second-order mesenteric arteries from Sprague Dawley rats. In addition, the acute hypotensive effect was evaluated in anesthetized rats infused with cumulative concentrations of the EM extract.Results: Both EM extract (10-4–1 mg/ml) and phenanthrene (10-7–10-4 M) relaxed endothelium-intact arteries, an effect that was partly reduced by endothelium removal (p < 0.001). A significant decrease in the relaxant effect of the extract and the phenanthrene was observed with L-NAME and apamin/charybdotoxin in endothelium-intact vessels, and with iberiotoxin in denuded vessels. SNP (sodium nitroprusside)-induced relaxation was significantly enhanced by EM extract and phenanthrene. By contrast, ODQ (1H-[1,2,4]oxadiazolo[4,3-a]quinoxaline-1-one), 4-aminopyridine and glibenclamide (endothelium-denuded vessels) and indomethacin (endothelium-intact vessels) had no effect. In calcium-free solution, both the EM extract and phenanthrene inhibited extracellular Ca2+-induced contraction in high KCl and phenylephrine (PE) pre-contracted rings. They also inhibited the intracellular Ca2+ release sensitive to PE. The acute infusion of EM extract (20 and 70 mg/kg) induced an immediate and transient dose-dependent hypotensive effect.Conclusion: The ethanolic extract of EM tubers and its main active compound, 1-(4′-hydroxybenzyl)-4,8-dimethoxyphenanthrene-2,7-diol (phenanthrene) induced vasorelaxant effects on rat resistance vessels, through pleiotropic effects including endothelium-dependent effects (NOS activation, enhanced EDH production) and endothelium-independent effects (opening of KCa channels, inhibition of Ca2+ channels, inhibition of intracellular Ca2+ release and PDE inhibition).
A double-blind randomized controlled trial was used to assess the comedogenic potential of the dermatological products containing d-Alpha tocopheryl acetate. A total of 15 healthy males (20–45 years old) with prominent follicular orifices and the ability to form comedones on the upper aspect of the back were enrolled. Each participant was given pads containing 4 test products. The positive control arm received a pad containing octyl palmitate which is a reported comedogenic material. The negative control arm received a pad without any test material. Participants were randomized to apply either the positive, negative or the active test cream to the application area for 4 weeks. Comedones were identified using epidermal biopsy under a stereomicroscope. The average number of microcomedone before exposure (baseline) with octyl palmitate was 6.1 ± 0.6 (mean ± SEM), and changed to 27.3 ± 4.7 which was more than 50% increase in comedone formation in every subject with the average change from base line was 365.4 ± 87.6%. In the negative control arm the average number of microcomedone at baseline was 6.4 ± 1.1 and at 4 week-application was 3.4 ± 0.6 (−43.0 ± 9.5% increased). All tested products produced less than a 50% increase in the number of microcomedones. Analyzed data from 12 subjects indicated non-comedogenic potential of the tested products containing-alpha tocopheryl acetate and other ingredients including lanolin, kernel oil and avocado oil and sunflower oil, etc. The octyl palmitate produced more than 50% increase in comedone formation in every analyzed subject.
The leaves of Aquilaria spp. promote “physiological balance”, and are “cardiotonic and provide blood nourishment”. In Asia, these leaves are increasingly consumed as tea and claimed to provide benefits to cardiovascular function, albeit without any scientific proof. Therefore, this study sought to evaluate the action of Aquilaria crassna leaf aqueous extract (AE) on vascular function and vascular smooth muscle cytotoxicity. AE and a main constituent, mangiferin were investigated for their vasorelaxation of rat mesenteric arteries and aortae in vitro . Acute cytotoxicity of AE (0.1–1000 μg/ml) and mangiferin (0.1–100 μM) on rat enzymatically isolated vascular smooth muscle cells was assayed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide. AE dilated rat mesenteric arteries (EC 50 ∼107 μg/ml, E max ∼95%) more than aorta (EC 50 ∼265 μg/ml, E max ∼76%, p < 0.05). AE-induced vasodilation in mesenteric artery was reduced by endothelial removal (EC 50 ∼202 μg/ml, p < 0.05), incubation with endothelial nitric oxide synthase (eNOS) (100 μM, L -NAME) (EC 50 ∼309 μg/ml, p < 0.05), and partly reduced by L-type Ca 2+ channel blockade at higher concentrations. Likewise, mangiferin (1–100 μM) dilated the mesenteric artery more potently than the aorta. However, its maximum relaxation was less than with AE (41% in the mesenteric artery and <10% in the aorta). Isolated vascular smooth muscle cells incubated in AE or mangiferin for 1 h showed no cytotoxicity. Thus, AE is a vasorelaxant while being free of acute cytotoxicity towards vascular smooth muscle, thus potentially ameliorating human vascular dysfunction.
Bacopa monnieri (L.) Wettst. (Brahmi) is a traditional memory enhancer partly by improved cerebral blood flow. Here we sought to link improved cognitive function with better blood flow in randomised double-blinded placebo-controlled trial in an elderly cohort. Normotensive Thais, aged 55-80y having mini-mental state examination (MMSE) scores > 25, no dementia or other psycho/neurological disease, normal lipid profile, and blood biochemistry were recruited. The trial design was a 2 week run-in, 12 week intervention of test product or placebo, and 4 week washout. The intervention was an extract of B. monnieri leaves (eBM) in 40 ml of mulberry juice. The placebo contained mulberry juice and other constituents to match gustatory properties. End-points were a battery of memory functions, carotid blood velocity, post-ischemic microvascular blood flow, markers of vascular inflammation, blood pressure and the blood markers. Response latency was reduced by 14.2 ± 4.9% (p = 0.022 comparing placebo) but only in > 65s. Other memory recall parameters were either unaffected or for ‘accuracy of recall’ was already maximal preventing further improvement. No change was detected in carotid blood velocity while microvascular blood flow marginally increased (by 28.4 ± 8.3%, p = 0.07). This preliminary evidence warrant further studies on selected patients with microvascular cognitive dysfunction using more discriminating protocols.
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