Arbuscular mycorrhizal fungi (AMF) actively colonize plant roots and thus enhance plant growth through different mechanisms. In the present study, trifoliate orange (Poncirus trifoliata) seedlings inoculated with Diversispora versiformis were subjected to 0 and 0.2 mmol/L sodium nitroprusside (SNP, a nitric oxide donor) treatments. After eight weeks, exogenous SNP considerably increased root mycorrhizal colonization by 25%, showing a positive stimulating effect of NO on mycorrhizal formation. Mycorrhizal inoculation significantly increased plant growth performance (height, stem diameter, leaf number and shoot and root dry weight) and root traits (length, projected area, surface area, volume and number of 2nd and 3rd order lateral roots) than non-mycorrhizal treatment and NO (exogenous SNP treatment) heavily strengthened the mycorrhizal effects. Moreover, NO and mycorrhization induced more fine root (0-0.5 cm) formation. There was an opposite changed trend in root sucrose and leaf and root glucose contents by SNP in AMF versus non-AMF seedlings. All these results implied that NO plays important roles in mycorrhizal formation and development and also accelerates mycorrhizal effects on plant growth and root development of trifoliate orange.
Lead (Pb) is one of the most abundant toxic heavy metals which adversely affected growth and yield of crop plants. Nitric oxide (NO), an endogenous signaling molecule, has been suggested to be involved in defense responses to biotic and abiotic stresses in plants. The present study was done to induce Pb tolerance in cowpea plants by exogenous NO application using two levels of Pb, 0 and 200 mg Pb (NO3)2 kg-1 soil and three NO levels, 0, 0.5 and 1 mM sodium nitroprusside (SNP), as NO donor. The results showed that Pb treatment caused a significant increase in Pb concentration in all plant parts. Roots had higher levels of Pb than the stems, leaves and seeds. Furthermore, lead toxicity reduced auxin (IAA), cytokinin and gibberellic acid (GA3) content but increased abscisic acid (ABA) level. Moreover Pb stress decreased stomatal conductance, leaf area and consequently seed yield of cowpea. Exogenous application of NO at 0.5 mM noticeably alleviated the lead toxicity by improving the leaf area, stomatal conductance and seed yield. NO increased Pb tolerance by lowering Pb uptake and translocation, enhancing the promoting phytohormone (IAA, cytokinin and GA3) level and reducing ABA content.
The aim of the present study was to determine the effect of nitric oxide (NO) on the production of prostaglandin E2 (PGE2) by a human osteoblast cell line (HOS cells) stimulated with hydroxyapatite. Cells were cultured on the HA surfaces with or without the presence of NO donors (SNAP and NAP) for 3 days. The effect of NO scavenger, carboxy PTIO, or endothelial nitric oxide synthase (eNOS) inhibitor, L-NIO, was assessed by adding this scavenger in the cultures of HA-stimulated HOS cells with or without the presence of SNAP. Furthermore, HOS cells were pre-treated with anti-human integrin alphaV antibody, indomethacin, a non-specific inhibitor, aspirin, a COX-1 inhibitor, or nimesulide, a COX-2 inhibitor, prior to culturing on HA surfaces with or without the presence of SNAP. The levels of PGE2 were determined from the 3 day culture supernatants. The results showed that the production of PGE2 by HA-stimulated HOS cells was augmented by SNAP. Carboxy PTIO suppressed but L-NIO only partially inhibited the production of PGE2 by HA-stimulated HOS cells with or without the presence of exogenous NO. Pre-treatment of the cells with anti-human integrin alphaV antibody, indomethacin or nimesulide but not aspirin suppressed the production of PGE2 by HA-stimulated HOS cells with or without the presence of NO. Therefore, the results of the present study suggest that NO may up-regulate the production of PGE2 by augmenting the COX-2 pathway initiated by the binding between HOS cell-derived integrin alphaV and HA surface.
The endothelial barrier function is tightly controlled by a broad range of signaling cascades including nitric oxide-cyclic guanosine monophosphate (NO-cGMP) pathway. It has been proposed that disturbances in NO and cGMP production could interfere with proper endothelial barrier function. In this study, we assessed the effect of interferon-gamma (IFN-gamma), a pro-inflammatory cytokine, on NO and cGMP levels and examined the mechanisms by which NO and cGMP regulate the IFN-gamma-mediated HUVECs hyperpermeability. The flux of fluorescein isothiocyanate-labeled dextran across cell monolayers was used to study the permeability of endothelial cells. Here, we found that IFN-gamma significantly attenuated basal NO concentration and the increased NO levels supplied by a NO donor, sodium nitroprusside (SNP). Besides, application of IFN-gamma also significantly attenuated both the basal cGMP concentration and the increased cGMP production donated by a cell permeable cGMP analogue, 8-bromo-cyclic GMP (8-Br-cGMP). In addition, exposure of the cell monolayer to IFN-gamma significantly increased HUVECs basal permeability. However, L-NAME pretreatment did not suppress IFN-gamma-induced HUVECs hyperpermeability. L-NAME pretreatment followed by SNP or SNP pretreatment partially reduced IFN-gamma-induced HUVECs hyperpermeability. Pretreatment with a guanylate cyclase inhibitor, 6-anilino-5,8-quinolinedione (LY83583), led to a further increase in IFN-gamma-induced HUVECs hyperpermeability. The findings suggest that the mechanism underlying IFN-gamma-induced increased HUVECs permeability is partly related to the inhibition of NO production.
Introduction: Eurycoma longifolia (E. longifolia) which is better known locally as Tongkat Ali is an indigenous plant in Malaysia. It belongs to the family of Simaroubaceae and is popular as a traditional medicine for its aphrodisiac properties. Throughout the years, several studies have been conducted to prove its effect on aphrodisiac action, antimalarial, antibacterial and anxiolytic properties but its effect to the cardiovascular system had not been fully explored. This study was aimed to demonstrate the changes that take place in the isolated heart following the injection of the extract. Methods: Three parameters that were measured included the coronary perfusion pressure (CPP), the left ventricular developed pressure (LVDP) and the heart rate (HR). Eighteen isolated rat hearts were used and were divided equally into three groups. The first group was to observe the effect of Isoprenaline, a β agonist while the second group was to see the effect of sodium nitroprusside (SNP), a nitric oxide (NO) donor. The dose which gave the maximum effect for these two positive controls was used to compare with the effect of E. longifolia water extract in the third group of rats. Isolated heart was mounted using the Langendorff apparatus and perfused with modified Krebs-Henseleit buffer. Doses of controls and the extract were instilled through an injection port, and the effect of each dose was monitored. Results: E. longifolia extract was found to reduce the CPP in normotensive rat at two of the highest doses. A dose of 1.0 mg of the extract reduced the CPP significantly from 34.52 ± 4.99 mmHg of the baseline value to 31.99 ± 4.93 mmHg while the dose of 10.0 mg of the extract reduced the CPP
significantly to 32.67 ± 3.89 mmHg. However, there were no significant changes of effect of the extract on the LVDP and HR as compared to control. Conclusion: These early findings suggest that E. longifolia extract may have vasodilatory property, which supports its traditional usage with minimum cardiovascular side effects.
The aim of the present study was to determine the effect of nitric oxide (NO) on the production of cyclic AMP (cAMP) by a human osteoblast cell line (HOS cells) stimulated with hydroxyapatite. Cells were cultured on the HA surfaces with or without the presence of NO donors (SNAP and NAP) for 3 days. The effect of adenylyl cyclase inhibitor (SQ22536), NO scavenger (carboxy PTIO) or endothelial nitric oxide synthase (eNOS) inhibitor (L-NIO), was assessed by adding these to the cultures of HA-stimulated HOS cells with or without the presence of SNAP. Furthermore, HOS cells were pre-treated with anti-human integrin alphaV antibody prior to culturing on HA surfaces with or without the presence of SNAP. The levels of cAMP and cGMP were determined from the 3-day culture supernatants. The results showed that the production of cAMP but not cGMP by HA-stimulated HOS cells was augmented by SNAP. SQ22536 and carboxy PTIO suppressed but L-NIO only partially inhibited the production of cAMP by HA-stimulated HOS cells with or without the presence of exogenous NO. Pre-treatment of the cells with anti-human integrin alphaV antibody suppressed the production of cAMP by HA-stimulated HOS cells with or without the presence of NO. Therefore, the results of the present study suggest that NO may up-regulate the production of cAMP, perhaps, by augmenting adenylyl cyclase activity initiated by the binding between HOS cell-derived integrin alphaV and HA surface.
BACKGROUND AND AIMS OF THE WORK: Nitric oxide (NO) has been reported to enhance the production of cAMP by hydroxyapatite (HA)-induced a human osteoblast cell line (HOS cells). The aim of the present study was to test the hypothesis that exogenous NO may up-regulate the proliferation of hydroxyapatite (HA)-induced HOS cells via the cyclic-AMP-protein kinase A (PKA) pathway.
Elevated nitric oxide (NO) has been associated with destructive periodontal disease. The aim of the present study was to test the hypothesis that exogenous NO may inhibit a protective immune response to Aggregatibacter actinomycetemcomitans lipopolysaccharide (LPS) in a murine model.