scholarly journals Postharvest UV-B Irradiation Stimulated Ginsenoside Rg1 Biosynthesis through Nitric Oxide (NO) and Jasmonic Acid (JA) in Panax quinquefolius Roots

Molecules ◽  
2019 ◽  
Vol 24 (8) ◽  
pp. 1462
Author(s):  
Jie Zhou ◽  
Zhi-fang Ran ◽  
Xiao-tong Yang ◽  
Jia Li
Keyword(s):  
Nitric Oxide ◽  
Jasmonic Acid ◽  
Signal Pathway ◽  
Panax Quinquefolius ◽  
Ginsenoside Rg1 ◽  
Drying Process ◽  
Synthesis Inhibitor ◽  
Nos Inhibitors ◽  
Underlying Mechanisms ◽  
Dependent Pathway

The study highlights the influence and signal transduction mechanism of postharvest UV-B on the production of Rg1 in Panax quinquefolius roots during the drying process. The results showed that postharvest UV-B irradiation induced generation of nitric oxide (NO), jasmonic acid (JA), and ginsenoside Rg1 of P. quinquefolius roots. The UV-B-induced increase of Rg1 was suppressed by NO-specific scavenger (cPTIO) and NOS inhibitors (PBITU), JA synthesis inhibitor (SHAM), and JA synthesis inhibitor (PrGall), indicating that NO and JA played essential parts in UV-B-induced Rg1. External NO inhibitors treatment inhibited UV-B-induced accumulation of NO and JA, which suggested that NO was located upstream of the JA signal pathway. NO-caused Rg1 was inhibited by SHAM and PrGall, implying JA participated in transmitting signal NO to Rg1 accumulation. In other words, NO mediated the postharvest UV-B-induced Rg1 accumulation by the JA-dependent pathway in P. quinquefolius roots during the drying process, which helps us understand the underlying mechanisms involved in UV-B-induced Rg1 production and provides information helpful for P. quinquefolius production.

scholarly journals Smoke-Isolated Karrikins Stimulated Tanshinones Biosynthesis in Salvia miltiorrhiza through Endogenous Nitric Oxide and Jasmonic Acid

Molecules ◽  
2019 ◽  
Vol 24 (7) ◽  
pp. 1229 ◽  
Author(s):  
Jie Zhou ◽  
Zi-xin Xu ◽  
Hui Sun ◽  
Lan-ping Guo
Keyword(s):  
Nitric Oxide ◽  
Signal Transduction ◽  
Jasmonic Acid ◽  
Hairy Root ◽  
Salvia Miltiorrhiza ◽  
Signal Molecules ◽  
Synthesis Inhibitor ◽  
Transduction Mechanism ◽  
Signal Transduction Mechanism ◽  
Nos Inhibitors

Although smoke-isolated karrikins (KAR1) could regulate secondary metabolism in medicinal plants, the signal transduction mechanism has not been reported. This study highlights the influence of KAR1 on tanshinone I (T-I) production in Salvia miltiorrhiza and the involved signal molecules. Results showed KAR1-induced generation of nitric oxide (NO), jasmonic acid (JA) and T-I in S. miltiorrhiza hairy root. KAR1-induced increase of T-I was suppressed by NO-specific scavenger (cPTIO) and NOS inhibitors (PBITU); JA synthesis inhibitor (SHAM) and JA synthesis inhibitor (PrGall), which indicated that NO and JA play essential roles in KAR1-induced T-I. NO inhibitors inhibited KAR1-induced generation of NO and JA, suggesting NO was located upstream of JA signal pathway. NO-induced T-I production was inhibited by SHAM and PrGall, implying JA participated in transmitting signal NO to T-I accumulation. In other words, NO mediated the KAR1-induced T-I production through a JA-dependent signaling pathway. The results helped us understand the signal transduction mechanism involved in KAR1-induced T-I production and provided helpful information for the production of S. miltiorrhiza hairy root.

Nitric oxide inhibits human and canine pulmonary vascular tone via a postjunctional, nonelectromechanical, cGMP-dependent pathway

1999 ◽  
Vol 77 (5) ◽  
pp. 320-329 ◽  
Author(s):  
Luke J Janssen ◽  
Kai Mardi ◽  
Stuart Netherton ◽  
Pierre-A. Betti
Keyword(s):  
Nitric Oxide ◽  
Soluble Guanylate Cyclase ◽  
Electrical Field Stimulation ◽  
Adrenergic Nerve ◽  
Synthesis Inhibitor ◽  
No Donor ◽  
Phasic Activity ◽  
Dependent Protein ◽  
Adrenergic Nerve Endings ◽  
Dependent Pathway

We examined nitric oxide mediated regulation of pulmonary arterial and venous smooth muscle (PASM and PVSM, respectively): whether this inhibition is mediated via prejunctional receptors on adrenergic nerve endings; whether NO is neuronally derived; the relationship between degree of inhibition and vessel size; and identification of the signalling mechanisms involved. Canine pulmonary vascular tissues were generally quiescent, while human PASM exhibited spontaneous phasic activity. The nitric oxide (NO) synthesis inhibitor Nω-nitro-L-arginine (L-NNA; 10-4M) increased tone and enhanced phasic activity. Electrical field stimulation (EFS) evoked contractions were markedly enhanced by L-NNA in an endothelium-dependent fashion, and antagonized by the NO donor S-nitroso-N-acetyl-penicillamine (SNAP; 10-7to 10-5M). 8-Bromo-cGMP mimicked the effects of SNAP on basal tone and EFS contractions, while an inhibitor of soluble guanylate cyclase mimicked those of L-NNA. While mechanical responses to exogenously added norepinephrine (10-9-10-4M) were also enhanced by L-NNA and suppressed by SNAP, EFS-evoked excitatory junction potentials were unaffected by SNAP. We conclude that, in human and canine PASM and PVSM, there is a tonic generation of NO originating within the endothelium that does not mediate a prejunctional effect, but which acts postjunctionally to activate a cGMP-dependent pathway within the smooth muscle.Key words: adrenergic neurotransmission, norepinephrine, regiospecificity, cGMP-dependent protein kinase.

scholarly journals Trichoderma asperelloides Suppresses Nitric Oxide Generation Elicited by Fusarium oxysporum in Arabidopsis Roots

2014 ◽  
Vol 27 (4) ◽  
pp. 307-314 ◽  
Author(s):  
Kapuganti J. Gupta ◽  
Luis A. J. Mur ◽  
Yariv Brotman
Keyword(s):  
Nitric Oxide ◽  
Fusarium Oxysporum ◽  
No Production ◽  
Disease Development ◽  
Necrotrophic Pathogen ◽  
Trichoderma Spp ◽  
Promote Plant Growth ◽  
Induced Genes ◽  
Underlying Mechanisms ◽  
Lectin Protein

Inoculations with saprophytic fungus Trichoderma spp. are now extensively used both to promote plant growth and to suppress disease development. The underlying mechanisms for both roles have yet to be fully described so that the use of Trichoderma spp. could be optimized. Here, we show that Trichoderma asperelloides effects include the manipulation of host nitric oxide (NO) production. NO was rapidly formed in Arabidopsis roots in response to the soil-borne necrotrophic pathogen Fusarium oxysporum and persisted for about 1 h but is only transiently produced (approximately 10 min) when roots interact with T. asperelloides (T203). However, inoculation of F. oxysporum–infected roots with T. asperelloides suppressed F. oxysporum–initiated NO production. A transcriptional study of 78 NO-modulated genes indicated most genes were suppressed by single and combinational challenge with F. oxysporum or T. asperelloides. Only two F. oxysporum–induced genes were suppressed by T. asperelloides inoculation undertaken either 10 min prior to or after pathogen infection: a concanavlin A-like lectin protein kinase (At4g28350) and the receptor-like protein RLP30. Thus, T. asperelloides can actively suppress NO production elicited by F. oxysporum and impacts on the expression of some genes reported to be NO-responsive. Of particular interest was the reduced expression of receptor-like genes that may be required for F. oxysporum–dependent necrotrophic disease development.

Effects of NG-nitro-L-arginine methyl ester on renal function and blood pressure

1991 ◽  
Vol 261 (6) ◽  
pp. F1033-F1037 ◽  
Author(s):  
V. Lahera ◽  
M. G. Salom ◽  
F. Miranda-Guardiola ◽  
S. Moncada ◽  
J. C. Romero
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Renal Function ◽  
Methyl Ester ◽  
Renal Plasma Flow ◽  
Urinary Sodium Excretion ◽  
Systemic Blood Pressure ◽  
Synthesis Inhibitor ◽  
Renal Changes ◽  
Dose Dependent

The dose-dependent effects of intravenous infusions of nitric oxide (NO) synthesis inhibitor, NG-nitro-L-arginine methyl ester (L-NAME; 0.1, 1, 10, and 50 micrograms.kg-1.min-1), were studied in anesthetized rats to determine whether the inhibitory actions of L-NAME are manifested primarily in alterations of renal function or whether they are the consequences of the increase in systemic blood pressure. Mean arterial pressure (MAP) was not altered by the intravenous L-NAME infusions of 0.1 and 1.0 microgram.kg-1.min-1. However, 0.1 microgram.kg-1.min-1 L-NAME induced a 30% decrease in urine flow rate (UV). The administration of 1.0 microgram.kg-1.min-1 L-NAME, in addition to decreasing UV, also decreased urinary sodium excretion (UNaV) and renal plasma flow (RPF). The intravenous L-NAME infusions of 10.0 and 50.0 microgram.kg-1.min-1 intravenous L-NAME infusions of 10.0 and 50.0 microgram.kg-1.min-1 produced significant increases in MAP that reversed the initial fall in UV and UNaV, despite decreasing RPF and glomerular filtration rate (GFR). The administration of L-arginine alone (10 micrograms.kg-1.min-1) did not modify any of the parameters measured, but it effectively prevented all the hemodynamic and renal changes induced by the infusion of 50 micrograms.kg-1.min-1 L-NAME. These results suggest that the decrease in nitric oxide production induced by the intravenous infusion of L-NAME affects renal excretion of sodium and water in the absence of any significant change in blood pressure. At larger doses, L-NAME also produces hypertension that overrides the initial antinatriuretic effect.

Atorvastatin attenuates the antinociceptive tolerance of morphine via nitric oxide dependent pathway in male mice

2016 ◽  
Vol 125 ◽  
pp. 173-180 ◽  
Author(s):  
Mahsa Hassanipour ◽  
Hossein Amini-Khoei ◽  
Hamed Shafaroodi ◽  
Armin Shirzadian ◽  
Nastaran Rahimi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Male Mice ◽  
Antinociceptive Tolerance ◽  
Dependent Pathway

scholarly journals Differential Induction of the Toll-Like Receptor 4-MyD88-Dependent and -Independent Signaling Pathways by Endotoxins

2005 ◽  
Vol 73 (5) ◽  
pp. 2940-2950 ◽  
Author(s):  
Susu M. Zughaier ◽  
Shanta M. Zimmer ◽  
Anup Datta ◽  
Russell W. Carlson ◽  
David S. Stephens
Keyword(s):  
Nitric Oxide ◽  
Signaling Pathways ◽  
Lipid A ◽  
Raw 264.7 ◽  
Receptor Complex ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Nitric Oxide Release ◽  
Tnf Α ◽  
Dependent Pathway

ABSTRACT The biological response to endotoxin mediated through the Toll-like receptor 4 (TLR4)-MD-2 receptor complex is directly related to lipid A structure or configuration. Endotoxin structure may also influence activation of the MyD88-dependent and -independent signaling pathways of TLR4. To address this possibility, human macrophage-like cell lines (THP-1, U937, and MM6) or murine macrophage RAW 264.7 cells were stimulated with picomolar concentrations of highly purified endotoxins. Harvested supernatants from previously stimulated cells were also used to stimulate RAW 264.7 or 23ScCr (TLR4-deficient) macrophages (i.e., indirect induction). Neisseria meningitidis lipooligosaccharide (LOS) was a potent direct inducer of the MyD88-dependent pathway molecules tumor necrosis factor alpha (TNF-α), interleukin-1β (IL-1β), monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 3α (MIP-3α), and the MyD88-independent molecules beta interferon (IFN-β), nitric oxide, and IFN-γ-inducible protein 10 (IP-10). Escherichia coli 55:B5 and Vibrio cholerae lipopolysaccharides (LPSs) at the same pmole/ml lipid A concentrations induced comparable levels of TNF-α, IL-1β, and MIP-3α, but significantly less IFN-β, nitric oxide, and IP-10. In contrast, LPS from Salmonella enterica serovars Minnesota and Typhimurium induced amounts of IFN-β, nitric oxide, and IP-10 similar to meningococcal LOS but much less TNF-α and MIP-3α in time course and dose-response experiments. No MyD88-dependent or -independent response to endotoxin was seen in TLR4-deficient cell lines (C3H/HeJ and 23ScCr) and response was restored in TLR4-MD-2-transfected human embryonic kidney 293 cells. Blocking the MyD88-dependent pathway by DNMyD88 resulted in significant reduction of TNF-α release but did not influence nitric oxide release. IFN-β polyclonal antibody and IFN-α/β receptor 1 antibody significantly reduced nitric oxide release. N. meningitidis endotoxin was a potent agonist of both the MyD88-dependent and -independent signaling pathways of the TLR4 receptor complex of human macrophages. E. coli 55:B5 and Vibrio cholerae LPS, at the same picomolar lipid A concentrations, selectively induced the MyD88-dependent pathway, while Salmonella LPS activated the MyD88-independent pathway.

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