In vitro study of antimicrobial effects of Rosmarinus officinalis and Glycyrrhiza glabra extracts against some pathogens

Background and aims: Disease causing bacteria have always been considered a major cause of morbidity and mortality in humans. The appearance of resistant microorganisms paved the way to the occurrence of infections that are only treated by a limited number of antimicrobial agents. The present study was, the antimicrobial effects of Rosmarinus officinalis and Glycyrrhiza glabra extract against some pathogens. Methods: In this study, the antibacterial activity using 9 Gram-positive and Gram-negative bacterial strains includes: Streptococcus pyogenes ATCC® 19615, Streptococcus pneumoniae ATCC 49619, S. saprophyticus ATCC®15305, Hafnia alvei ATCC 51873, Acinetobacter baumannii ATCC 19606, Enterococcus faecalis ATCC 29212, Proteus mirabilis ATCC 35659, Serratia marcescens ATCC 274 and Staphylococcus aureus ATCC® 25923 with micro dilution methods was studied. The MIC, MBC were studied also, resistance of these bacteria to standard antibiotics such as erythromycin, cefixime, ceftazidime, tetracycline, ampicillin and amikacin were compared. Results: In this study, the minimum inhibitory concentration (MIC) was used. The levels of MIC of R. officinalis were in ranges from 6.25 to 25 mg/ml. The highest MIC value was observed at 25 ppm against S. pyogenes, S. pneumoniae and P. mirabilis and the levels of MIC of G. glabra were in ranges from 6.25 to 12.5 ppm. The highest MIC value was observed at 12.5 ppm against S. pyogenes, S. pneumoniae, P. mirabilis and S. marcescens. Conclusion: In important human pathogens, drug resistance is increasing according to the results of this study, and may be proposed that this plant can be used as a drug. It can be a good way to replace herbs with chemical drugs

Genetic fuzzy system predicting contractile reactivity patterns of small arteries

Monitoring of physiological surrogate end points in drug development generates dynamic time-domain data reflecting the state of the biological system. Conventional data analysis often reduces the information in these data by extracting specific data points, thereby discarding potentially useful information. We developed a genetic fuzzy system (GFS) algorithm that is capable of learning all information in time-domain physiological data. Data on isometric force development of isolated small arteries were used as a framework for developing and optimizing a GFS. GFS performance was improved by several strategies. Results show that optimized fuzzy systems (OFSs) predict contractile reactivity of arteries accurately. In addition, OFSs identified significant differences that were undetectable using conventional analysis in the responses of arteries between groups. We concluded that OFSs may be used in clustering or classification tasks as aids in the objective identification or prediction of dynamic physiological behavior

Hepatic oxidative stress, genotoxicity and vascular dysfunction in lean or obese zucker rats

Metabolic syndrome is associated with increased risk of cardiovascular disease, which could be related to oxidative stress. Here, we investigated the associations between hepatic oxidative stress and vascular function in pressurized mesenteric arteries from lean and obese Zucker rats at 14, 24 and 37 weeks of age. Obese Zucker rats had more hepatic fat accumulation than their lean counterparts. Nevertheless, the obese rats had unaltered age-related level of hepatic oxidatively damaged DNA in terms of formamidopyrimidine DNA glycosylase (FPG) or human oxoguanine DNA glycosylase (hOGG1) sensitive sites as measured by the comet assay. There were decreasing levels of oxidatively damaged DNA with age in the liver of lean rats, which occurred concurrently with increased expression of Ogg1. The 37 week old lean rats also had higher expression level of Hmox1 and elevated levels of DNA strand breaks in the liver. Still, both strain of rats had increased protein level of HMOX-1 in the liver at 37 weeks. The external and lumen diameters of mesenteric arteries increased with age in obese Zucker rats with no change in media cross-sectional area, indicating outward re-modelling without hypertrophy of the vascular wall. There was increased maximal response to acetylcholine-mediated endothelium-dependent vasodilatation in both strains of rats. Collectively, the results indicate that obese Zucker rats only displayed a modest mesenteric vascular dysfunction, with no increase in hepatic oxidative stress-generated DNA damage despite substantial hepatic steatosis

Pulmonary exposure to carbon black nanoparticles and vascular effects

<p>Abstract</p> <p>Background</p> <p>Exposure to small size particulates is regarded as a risk factor for cardiovascular diseases.</p> <p>Methods</p> <p>We exposed young and aged apolipoprotein E knockout mice (<it>apoE^-/-</it>) to carbon black (Printex 90, 14 nm) by intratracheal instillation, with different dosing and timing, and measured vasomotor function, progression of atherosclerotic plaques, and VCAM-1, ICAM-1, and 3-nitrotyrosine in blood vessels. The mRNA expression of <it>VCAM-1</it>, <it>ICAM-1</it>, <it>HO-1</it>, and <it>MCP-1 </it>was examined in lung tissue.</p> <p>Results</p> <p>Young <it>apoE^-/-</it>mice exposed to two consecutive 0.5 mg/kg doses of carbon black exhibited lower acetylcholine-induced vasorelaxation in aorta segments mounted in myographs, whereas single doses of 0.05-2.7 mg/kg produced no such effects. The phenylephrine-dependent vasocontraction response was shifted toward a lower responsiveness in the mice exposed once to a low dose for 24 hours. No effects were seen on the progression of atherosclerotic plaques in the aged <it>apoE^-/-</it>mice or on the expression of VCAM-1 and ICAM-1 and the presence of 3-nitrotyrosine in the vascular tissue of either young or aged <it>apoE^-/-</it>mice. The expression of <it>MCP-1 </it>mRNA was increased in the lungs of young <it>apoE^-/-</it>mice exposed to 0.9-2.7 mg/kg carbon black for 24 hours and of aged <it>apoE^-/-</it>mice exposed to two consecutive 0.5 mg/kg doses of carbon black seven and five weeks prior to sacrifice.</p> <p>Conclusion</p> <p>Exposure to nano-sized carbon black particles is associated with modest vasomotor impairment, which is associated neither with nitrosative stress nor with any obvious increases in the expression of cell adhesion proteins on endothelial cells or in plaque progression. Evidence of pulmonary inflammation was observed, but only in animals exposed to higher doses.</p

Modest vasomotor dysfunction induced by low doses of C60 fullerenes in apolipoprotein E knockout mice with different degree of atherosclerosis

<p>Abstract</p> <p>Background</p> <p>Exposure to small size particulate matter in urban air is regarded as a risk factor for cardiovascular effects, whereas there is little information about the impact on the cardiovascular system by exposure to pure carbonaceous materials in the nano-size range. C₆₀fullerenes are nano-sized particles that are expected to have a widespread use, including cosmetics and medicines.</p> <p>Methods</p> <p>We investigated the association between intraperitoneal injection of pristine C₆₀fullerenes and vasomotor dysfunction in the aorta of 11–13 and 40–42 weeks old apolipoprotein E knockout mice (apoE^-/-) with different degree of atherosclerosis.</p> <p>Results</p> <p>The aged apoE^-/-mice had lower endothelium-dependent vasorelaxation elicited by acetylcholine in aorta segments mounted in myographs and the phenylephrine-dependent vasoconstriction response was increased. One hour after an intraperitoneal injection of 0.05 or 0.5 mg/kg of C₆₀fullerenes, the young apoE^-/-mice had slightly reduced maximal endothelium-dependent vasorelaxation. A similar tendency was observed in the old apoE^-/-mice. Hampered endothelium-independent vasorelaxation was also observed as slightly increased EC₅₀of sodium nitroprusside-induced vasorelaxation response in young apoE^-/-mice.</p> <p>Conclusion</p> <p>Treatment with C₆₀fullerenes affected mainly the response to vasorelaxation in young apoE^-/-mice, whereas the vasomotor dysfunction in old apoE^-/-mice with more advanced atherosclerosis was less affected by acute C₆₀fullerene treatment. These findings represent an important step in the hazard characterization of C₆₀fullerenes by showing that intraperitoneal administration is associated with a moderate decrease in the vascular function of mice with atherosclerosis.</p

Modest effect on plaque progression and vasodilatory function in atherosclerosis-prone mice exposed to nanosized TiO2

<p>Abstract</p> <p>Background</p> <p>There is growing evidence that exposure to small size particulate matter increases the risk of developing cardiovascular disease.</p> <p>Methods</p> <p>We investigated plaque progression and vasodilatory function in apolipoprotein E knockout (<it>ApoE</it>^-/-) mice exposed to TiO₂. <it>ApoE</it>^-/-mice were intratracheally instilled (0.5 mg/kg bodyweight) with rutile fine TiO₂(fTiO₂, 288 nm), photocatalytic 92/8 anatase/rutile TiO₂(pTiO₂, 12 nm), or rutile nano TiO₂(nTiO₂, 21.6 nm) at 26 and 2 hours before measurement of vasodilatory function in aorta segments mounted in myographs. The progression of atherosclerotic plaques in aorta was assessed in mice exposed to nanosized TiO₂(0.5 mg/kg bodyweight) once a week for 4 weeks. We measured mRNA levels of <it>Mcp-1</it>, <it>Mip-2</it>, <it>Vcam-1</it>, <it>Icam-1 </it>and <it>Vegf </it>in lung tissue to assess pulmonary inflammation and vascular function. TiO₂-induced alterations in nitric oxide (NO) production were assessed in human umbilical vein endothelial cells (HUVECs).</p> <p>Results</p> <p>The exposure to nTiO₂was associated with a modest increase in plaque progression in aorta, whereas there were unaltered vasodilatory function and expression levels of <it>Mcp-1</it>, <it>Mip-2</it>, <it>Vcam-1</it>, <it>Icam-1 </it>and <it>Vegf </it>in lung tissue. The <it>ApoE^-/-</it>mice exposed to fine and photocatalytic TiO₂had unaltered vasodilatory function and lung tissue inflammatory gene expression. The unaltered NO-dependent vasodilatory function was supported by observations in HUVECs where the NO production was only increased by exposure to nTiO₂.</p> <p>Conclusion</p> <p>Repeated exposure to nanosized TiO₂particles was associated with modest plaque progression in <it>ApoE^-/-</it>mice. There were no associations between the pulmonary TiO₂exposure and inflammation or vasodilatory dysfunction.</p

Vasomotor function in rat arteries after ex vivo and intragastric exposure to food-grade titanium dioxide and vegetable carbon particles

Abstract Background Humans are continuously exposed to particles in the gastrointestinal tract. Exposure may occur directly through ingestion of particles via food or indirectly by removal of inhaled material from the airways by the mucociliary clearance system. We examined the effects of food-grade particle exposure on vasomotor function and systemic oxidative stress in an ex vivo study and intragastrically exposed rats. Methods In an ex vivo study, aorta rings from naïve Sprague-Dawley rats were exposed for 30 min to food-grade TiO2 (E171), benchmark TiO2 (Aeroxide P25), food-grade vegetable carbon (E153) or benchmark carbon black (Printex 90). Subsequently, the vasomotor function was assessed in wire myographs. In an in vivo study, lean Zucker rats were exposed intragastrically once a week for 10 weeks to vehicle, E171 or E153. Doses were comparable to human daily intake. Vasomotor function in the coronary arteries and aorta was assessed using wire myographs. Tetrahydrobiopterin, ascorbate, malondialdehyde and asymmetric dimethylarginine were measured in blood as markers of oxidative stress and vascular function. Results Direct exposure of E171 to aorta rings ex vivo increased the acetylcholine-induced vasorelaxation and 5-hydroxytryptamine-induced vasocontraction. E153 only increased acetylcholine-induced vasorelaxation, and Printex 90 increased the 5-hydroxytryptamine-induced vasocontraction, whereas Aeroxide P25 did not affect the vasomotor function. In vivo exposure showed similar results as ex vivo exposure; increased acetylcholine-induced vasorelaxation in coronary artery segments of E153 and E171 exposed rats, whereas E171 exposure altered 5-hydroxytryptamine-induced vasocontraction in distal coronary artery segments. Plasma levels of markers of oxidative stress and vascular function showed no differences between groups. Conclusion Gastrointestinal tract exposure to E171 and E153 was associated with modest albeit statistically significant alterations in the vasocontraction and vasorelaxation responses. Direct particle exposure to aorta rings elicited a similar type of response. The vasomotor responses were not related to biomarkers of systemic oxidative stress