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The aqueous extract from Berberis vulgaris fruit (B.V.) was tested to evaluate its antihypertensive effects on DOCA-induced hypertension in the rats. Hypertension was induced in male Sprague-Dawley rats (200-250 g) by DOCA-salt injection (20 mg/kg, twice weekly, for 5 weeks, s.c.) plus NaCl (1%) which was added to the animals' drinking water. Then 5 weeks later, the rats were anaesthetized with thiopental (30 mg/kg, i.p.) and the arterial blood pressure was measured. The mean arterial blood pressure and heart rate were 231 +/- 6.4 (mmHg) and 506 +/- 12 (beats/min), respectively. Administration of B.V. extracts significantly reduced the rat arterial blood pressure. In in vitro studies, rings of descending aorta were cut and mounted for isometric tension recording in an organ chamber containing Krebs solution. Mesenteric beds were also removed and perfused with Krebs solution. After 1 h of stabilization, preparations (aortic rings or mesenteric beds) were precontracted with phenylephrine (10(-5) M), then different concentrations of B.V. (0.4, 2 and 4 mg/mL) were added which caused a relaxation in these vessels. To investigate the mechanism of action of the extract, the tissues were incubated with either L-NAME (10(-5) M) or indomethacin (10(-5) M) for 20 min. In the aortic rings L-NAME pretreatment could only reduce the vasodilatory effects of a low concentration of B.V. (0.4 mg/mL), but indomethacin was without effect. In isolated perfused mesenteric beds preincubation with either L-NAME or indomethacin did not modify the vasodilator effects of the aqueous extract from B.V. fruit. The present results suggest that the antihypertensive and vasodilatory effects of B.V. fruit extract are mainly endothelial-independent and it may be used to treat hypertension, a status with endothelial dysfunction.

The use of natural products is very common among non-industrialized societies because these remedies are more accessible and affordable than modern pharmaceuticals. In developed countries, use of herbal products has recently increased as scientific evidence about their effectiveness has become broadly available. For the past two decades many research articles in the field of ethno-pharmacology have focused on the anti-diabetic effects of some natural products. This dramatic increase of interest was partly due to the fact that type 2 diabetes mellitus (T2DM) was considered as becoming a global epidemic health problem which imposed high cost to national health services around the world. We have no intention to advocate for replacing conventional pharmacotherapy with natural products to prevent and control T2DM. However, the fact that a lack of highly effective drug-therapy with existing synthetic agents and their resulting adverse effects motivated further search into traditional medicine in order to re-evaluate old remedies as well as screening to find new natural entities to be used as anti-diabetic products cannot be ignored. Some recent reports on the natural products with anti-diabetic effects have provided evidence for possible mechanisms of action. Nonetheless, the majority of investigators only speculated on a wide range of possible mechanisms or simply demonstrated an anti-hyperglycemic effect for the crude plant extracts or the isolated compounds of interest. A few reviews with less attention paid to mechanisms of action have been published on medicinal plants and diabetes. This article reviews publications on anti-diabetic natural products that have appeared in PUBMED or other research-related literature found on the Internet (from 1990 to present) to categorize them based on their mechanisms of action. We hope that this communication will be beneficial as a starting point to consider the discussed products for further investigations to identify and develop new remedies with potential alternative or complementary use in controlling T2DM.

17b-Estradiol receptors have been found in several brain nuclei including the suprachiasmatic nucleus (SCN) of mammalian species. The SCN is believed to act as brain clock regulating circadian and circannual biological rhythms, such as body temperature, sleep, and mood. Here, we examined whether 17b-estradiol (E 2 ) could affect cell excitability and synaptic transmission in the SCN. Bath application of E 2 (0.03-3 mM) increased the spontaneous firing frequency and depolarized cell membrane of the SCN neurons significantly. Furthermore, E 2 (0.03-3 mM) increased (by about 25-150% of control) frequency of the miniature excitatory postsynaptic currents. Amplitude of the evoked excitatory postsynaptic currents was enhanced (by about 32% of control) after exposure to 1 mM E 2 . The paired-pulse ratio was reduced by E 2 . These effects were prevented by the estrogen receptor antagonist, ICI 182780. Exposure to the biologically inactive 17a-estradiol did not cause any significant changes in the parameters mentioned above. These findings are in favor of an implication of estrogen in modulation of neuronal activity in SCN and possibly regulating circadian rhythms.

BackgroundOptimal pancreatic β-cell function is essential for the regulation of glucose homeostasis in both humans and animals and its impairment leads to the development of diabetes. Type 2 diabetes is a polygenic disease aggravated by environmental factors such as low physical activity or a hypercaloric high-fat diet.ResultsFree fatty acids represent an important factor linking excess fat mass to type 2 diabetes. Several studies have shown that chronically elevated free fatty acids have a negative effect on β-cell function leading to elevated insulin secretion basally but with an impaired response to glucose. The transcription factors PPARα, PPARγ and SREBP-1c respond to changing fat concentrations in tissues, thereby coordinating the genomic response to altered metabolic conditions to promote either fat storage or catabolism. These transcription factors have been identified in β-cells and it appears that each may exert influence on β-cell function in health and disease.ConclusionThe role of the PPARs and SREBP-1c as potential mediators of lipotoxicity is an emerging area of interest.