[Effects of testosterone and growth hormone on plasma concentrations of orexin in diet restricted rams]

It has been established that multiple neuroendocrine factors such as orexin operate as metabolic signals for the reproductive tract. Since the effects of testosterone and growth hormone on concentration of orexin in rams have not been studied, the goal of this study was to determine the effect of testosterone and growth hormone on mean plasma concentrations of orexin in rams fed restricted diets. Rams were randomly divided into 2 groups. Animals in first group were fed 100% of their required daily food and those in the second group were fed 50% of food fed to the first group for 10 days. Consequently, the rams in all groups received 6microg /Kg BW testosterone on days 7 and 8 and 6microg /Kg BW Testosterone and 5 microg /Kg BW growth hormone on days 9 and 10 of the experiment. Blood samples were collected from the jugular veins at -120 and +120 minutes of infusions. for orexin assay, Plasma orexin were measured by a homologous double-antibody radioimmunoassay [RIA]. Injection of different dosages of testosterone and combination of testosterone and growth hormone in the 50%-diet, significantly [P<0.05*] increased the mean plasma concentrations of orexin, while in the 100%-diet this had no effect. Results indicate that testosterone and growth hormone may increase mean concentrations of orexin in animals fed lower than their daily food requirement

Inhibitory effects of crataegus curviseoala, salvia hydrangea, and betula pendula on in-vitro protein glycosylation

Diabetes is one of the most common endocrine diseases spreading rapidly in the world. Diabetes complications are classified into acute and chronic. Non-enzymatic glycosylation of body proteins such as hemoglobin and albumin is the main cause of pathogenesis in chronic complications of diabetes. Protein glycosylation is an oxidative reaction. Antioxidants such as vitamin C may be able to reduce the chronic complications of diabetes through inhibiting protein glycosylation. The inhibitory effects of vitamin C and the polyphenolic extracts of Betula pendula, Saliva hydrangea and Crataegus curvisepala on the extent of glycosylation of albumin, insulin and hemoglobin were investigated in this study. Polyphenolic extracts of the aforesaid plants were prepared at three different concentrations, namely 3.6, 1.8 and 0.9 mg/ml. Vitamin C solutions were also prepared at 5 concentrations, namely 0.5, 5, 10, 50 and 500 micro g/ml. The highest extent of glycosylation inhibition of albumin and insulin was due to S. hydrangea by 100% and 97%, respectively, and that of hemoglobin was due to B. pendula by 80%. At its highest concentration, vitamin C inhibited the glycosylation of insulin, albumin and hemoglobin by 100%, 93%, and 58% respectively [P<0.05]. Based on our findings, the studied plants might be able to prevent the chronic complications of diabetes

[Cardiovascular effects of five native plants from southern of Khorasan state]

Traditionally, medicinal plants have been used to treat many diseases. To investigate the effects of different plants extract on cardiovascular system, five native southern Khorasan plants were used. Different concentration from the decoction of ziziphora, achillea millefolium [A.M] and aqueous extract of valeriana officinalis [V.O], viola and peganum harmala [P.H] were made]. Animals, Male Sprague Dawley rats [200-250 g, n=25] were anaesthetized with sodium thiopental [30 mg/kg, i.p.], then systemic arterial blood pressure [systolic, diastolic and mean] was measured. Mean arterial blood pressure was 140 +/- 5 mmHg. Intravenous administration of extract reduced the arterial blood pressure [eg. Administration of 0.03 mg/kg of aqueous extract of valeriana officinialis changed the blood pressure from 140 +/- 5 to 77 +/- 10 mmHg, P<0.0001]. There was a non-significant bradycardia with the administration of this extract. These results show that extract of ziziphora, V.O and A.M have hypotensive effects in the control rats and the most potent is V.O. By attention to non significant effect of these extract on heart rate, it is suggested that their hypotensive effect is induced by depletion in peripheral vascular resistance. For investigate of possible mechanism on vascular resistance, the isolated thorasic aorta rings in male rat were used. Therefore in another sets of experiments, after measuring blood pressure, chest was expanded and thoracic aorta was removed and cut into rings [3-4 mm]. Aqueous extract of V.O, in isolated aortic rings which was contracted by phenyl ephrin relaxed. Incubation of tissue with L-NAME [10[-5] molar] for 20 minutes significantly increased the response to different concentration of extract. Thus the vasodilatory mechanism of V.O is nondependent endothelium manner but it accomplish by vascular smooth muscle relaxation. In future, the effects of these extracts will be studied in the hypertensive rats, so that in case obtaining the same results and safety proof, these studied in the hypertensive rats, so that in case obtaining the same results and safety proof, these extracts on other systems, we can recommend take of these plant accompaniment by other treatment

[Effects of protein kinase C inhibitor on the responses to the vasodilator agents in the isolated aorta and mesenteric bed from hypertensive rats]

Numerous in vitro studies indicate that endothelium-mediated relaxation is reduced with development of hypertension. Considering the role of protein kinases in many metabolic processes of phosphate transferring and its importance in the cell communication and function [in the physiological and pathological states] and also the absence of any reports on the effects of these enzymes in the mediating responses to vasodilators during hypertension, this study became of interest. The objectives of this study were to measure the vascular responses to acetylcholine [ACh] and sodium nitroprusside [SNP] in the isolated rat aorta and mesenteric bed removed either from hypertensive or control rats and also to investigate the role of protein kinase C in these responses. Hypertension was induced in the male Sprague-Dawley rats [200-250 g] by DOCA-salt injection [20 mg/kg, twice weekly, for 5 weeks, s.c.] and NaCl [1%] was added to their drinking water. Control rats received saline injection [0.5 ml/kg, twice weekly, for 5 weeks, s.c.]. 5 weeks later, animals were anaesthetized with thiopental [30 mg/kg, i.p.], and arterial blood pressure was directly measured. Mean arterial blood pressure in control and hypertensive rats were: 98+/-7.5, 163 +/- 3.5, mmHg, respectively [P < 0.0001]. In in vitro studies, rings of descending aorta were cut and mounted for isometric tension recording in an organ chamber containg Krebs solution. After 1 h of stabilization, rings were precontracted with phenylephrine [5 x or 1 0-6 or 10-6 M], then concentration response curve to acetylcholine [ACh,-10-6 - 10-3 M] and SNP -10-8 - 10-4 M] were constructed. There was a significant decrease in response to Ach and also a reduction in the maximal response in rings isolated from hypertensive rats. Mesenteric beds were also removed either from control or hypertensive rats and perhsed with Krebs solution. After 1 h of stabilization, tissue were precontracted with norademalin M], then concentration-response curve to ACh [l0-8 - 10-4 M] and SNP [l0-8 - 10-4 M] were constructed. Responses to ACh but not to SNP were significantly reduced in tissue removed from hypertensive rats [eg. in response to l0-6 M of ACh: control: 41.6 +/- 4.9 hypertensive: 17.2 +/- 3.6 mmHg, P < 0.05]. However, addition of chelerythrine [l0 micro M], a protein kinase C [PKC] inhibitor, to the organ bath significantly restored these impaired responses. These results suggest that protein kinase C is involved in the endothelial dysfunction induced by hypertension

[ effects of genistein, a tyrosine kinase inhibitor, on acute and chronic inflammation in diabetic mice]

The effects of tyrosine kinases on acute and chronic inflammation during diabetes are not fully determined. Therefore, the present study focuses on investigating the effects of genistein, a tyrosine kinase inhibitor, on acute and chronic inflammation in diabetic mice. The mice either received normal saline [control, 0.1 ml, i.p., n=144] or were injected with streptozotocin [diabetic, STZ, 200 mg kg -1, i.p., n=144]. By injecting carrageenan and implanting 2 cotton pellets [a week after the injection of saline or STZ] we induced acute and chronic inflammation. Before injecting carrageenan or 5 day after implantation, 9 mice from each group [control or diabetic] received genistein [10 mg kg -1, i.p.], indomethacin [2 mg kg -1, i.p.] or L-NAME [0.1 mg kg -1, i.p.]. Paw edema and the weight of cotton pellets were significantly higher in diabetic mice. Pretreatment with either indomethacin or L NAME significantly reduced the acute and chronic inflammation in the diabetic group. Genistein reduced chronic inflammation significantly [P<0.0001]. These results suggest that activation of tyrosine kinases as well as prostaglandins and nitric oxide pathways are involved in the increased chronic inflammatory responses observed in the diabetic animals

[Effect of lovastatin on acetylcholine induced relaxation in the isolated mesenteric bed of streptozotocin diabetic rats]

We have investigated the acute effect of lovastatin on diabetes-induced endothelial dysfunction in the isolated mesenteric bed of streptozotocin-diabetic [STZ] rats. The endothelial function was tested in constantly perfused preparations isolated from rats, 12 weeks after treatment with ST2 [45 mg kg, i.p.].All preparations were precontracted by Phenylephrine 10-4M .Acetylcholine [ACh] induce relaxation in perfused mesenteric bed dose dependently. Response to Ach was reduced in diabetic group significantly. Co-perfusion with lovastatin [10-5 M, for 15 min] significantly improved the Ach-mediated relaxation removed from diabetic but not control rats. However, this beneficial effects of lovastatin was inhibited by pre-incubation of tissue with L-NAME [5 x 10-7 M, for 20 min], but not indomethacin [10-5 M] the vasodilatory responses to sodium nitroprusside from control or diabetic rats were unchanged by lovastatin pretreatment. From the present results it may conclude that lovastatin significantly improves endothelial-dependent relaxation in diabetic group. It could be via increasing nitric oxide bioavalibity, most probably due to its antioxidant effects