scholarly journals Effects of chitosan on nitric oxide production and inducible nitric oxide synthase activity and mRNA expression in weaned piglets

2018 ◽  
Vol 60 (No. 8) ◽  
pp. 359-366
Author(s):  
J. Li ◽  
B. Shi ◽  
S. Yan ◽  
L. Jin ◽  
Y. Guo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mrna Expression ◽  
Inducible Nitric Oxide Synthase ◽  
No Production ◽  
Weaned Piglets ◽  
Inos Activity ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

The effects of chitosan on nitric oxide (NO) production and inducible nitric oxide synthase (iNOS) activity and gene expression in vivo or vitro were investigated in weaned piglets. In vivo, 180 weaned piglets were assigned to five dietary treatments with six replicates. The piglets were fed on a basal diet supplemented with 0 (control), 100, 500, 1000, and 2000 mg chitosan/kg feed, respectively. In vitro, the peripheral blood mononuclear cells (PBMCs) from a weaned piglet were cultured respectively with 0 (control), 40, 80, 160, and 320 µg chitosan/ml medium. Results showed that serum NO concentrations on days 14 and 28 and iNOS activity on day 28 were quadratically improved with increasing chitosan dose (P < 0.05). The iNOS mRNA expressions were linearly or quadratically enhanced in the duodenum on day 28, and were improved quadratically in the jejunum on days 14 and 28 and in the ileum on day 28 (P < 0.01). In vitro, the NO concentrations, iNOS activity, and mRNA expression in unstimulated PBMCs were quadratically enhanced by chitosan, but the improvement of NO concentrations and iNOS activity by chitosan were markedly inhibited by N-(3-[aminomethyl] benzyl) acetamidine (1400w) (P < 0.05). Moreover, the increase of NO concentrations, iNOS activity, and mRNA expression in PBMCs induced by lipopolysaccharide (LPS) were suppressed significantly by chitosan (P < 0.05). The results indicated that the NO concentrations, iNOS activity, and mRNA expression in piglets were increased by feeding chitosan in a dose-dependent manner. In addition, chitosan improved the NO production in unstimulated PBMCs but inhibited its production in LPS-induced cells, which exerted bidirectional regulatory effects on the NO production via modulated iNOS activity and mRNA expression.

scholarly journals Induction of inducible nitric oxide synthase (iNOS) in vitro and in vivo brain microgllia

1996 ◽  
Vol 108 (supplement) ◽  
pp. 115-120
Author(s):  
Yoshihisa KITAMURA ◽  
Hideaki TAKAHASHI ◽  
Yasuji MATSUOKA ◽  
Yasuyuki NOMURA ◽  
Takashi TANIGUCHI
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

scholarly journals virB-Mediated Survival of Brucella abortus in Mice and Macrophages Is Independent of a Functional Inducible Nitric Oxide Synthase or NADPH Oxidase in Macrophages

2002 ◽  
Vol 70 (9) ◽  
pp. 4826-4832 ◽  
Author(s):  
Yao-Hui Sun ◽  
Andreas B. den Hartigh ◽  
Renato de Lima Santos ◽  
L. Garry Adams ◽  
Renée M. Tsolis
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Nadph Oxidase ◽  
Inducible Nitric Oxide Synthase ◽  
Brucella Abortus ◽  
In Vivo Models ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

ABSTRACT The Brucella abortus virB locus is required for establishing chronic infection in the mouse. Using in vitro and in vivo models, we investigated whether virB is involved in evasion of the bactericidal activity of NADPH oxidase and the inducible nitric oxide synthase (iNOS) in macrophages. Elimination of NADPH oxidase or iNOS activity in macrophages in vitro increased recovery of wild-type B. abortus but not recovery of a virB mutant. In mice lacking either NADPH oxidase or iNOS, however, B. abortus infected and persisted to the same extent as it did in congenic C57BL/6 mice up until 60 days postinfection, suggesting that these host defense mechanisms are not critical for limiting bacterial growth in the mouse. A virB mutant did not exhibit increased survival in either of the knockout mouse strains, indicating that this locus does not contribute to evasion of nitrosative or oxidative killing mechanisms in vivo.

Regulation and expression of inducible nitric oxide synthase in vitro and in vivo

1994 ◽  
Vol 109 (1-2) ◽  
pp. 107
Author(s):  
U. Malo-Ranta ◽  
J. Luoma ◽  
M. Laukkanen ◽  
T. Nikkari ◽  
S. Yla¨-Herttuala
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

scholarly journals Tissue expression of inducible nitric oxide synthase is closely associated with resistance to Leishmania major.

1994 ◽  
Vol 180 (3) ◽  
pp. 783-793 ◽  
Author(s):  
S Stenger ◽  
H Thüring ◽  
M Röllinghoff ◽  
C Bogdan
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Leishmania Major ◽  
Tissue Expression ◽  
Ifn Gamma ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

Previous studies with inhibitors of inducible nitric oxide synthase (iNOS) suggested that high-output production of nitric oxide (NO) is an important antimicrobial effector pathway in vitro and in vivo. Here, we investigated the tissue expression of iNOS in mice after infection with Leishmania major. Immunohistochemical staining with an iNOS-specific antiserum revealed that in the cutaneous lesion and draining lymph nodes (LN) of clinically resistant mice (C57BL/6), iNOS protein is found earlier during infection and in significantly higher amounts than in the nonhealing BALB/c strain. Similar differences were seen on the mRNA level as quantitated by competitive polymerase chain reaction. Anti-CD4 treatment of BALB/c mice not only induced resistance to disease, but also restored the expression of iNOS in the tissue. In situ, few or no parasites were found in those regions of the skin lesion and the draining LN which were highly positive for iNOS. By double labeling experiments, macrophages were identified as iNOS expressing cells in vivo. In the lesions of BALB/c mice, cells staining positively for transforming growth factor beta (TGF-beta), a potent inhibitor of iNOS in vitro, were strikingly more prominent than in C57BL/6, whereas no such difference was found for interleukin 4 or interferon gamma (IFN-gamma). In vitro, production of NO was approximately threefold higher in C57BL/6 than in BALB/c macrophages after stimulation with IFN-gamma. We conclude that the pronounced expression of iNOS in resistant mice is an important mechanism for the elimination of Leishmania in vivo. The relative lack of iNOS in susceptible mice might be a consequence of macrophage deactivation by TGF-beta and reduced responsiveness to IFN-gamma.

Inhibition of inducible nitric oxide synthase in vitro and in vivo by a water-soluble extract of Wendita calysina leaves

2007 ◽  
Vol 375 (6) ◽  
pp. 349-358 ◽  
Author(s):  
Stefania Marzocco ◽  
Anna Lisa Piccinelli ◽  
Luca Rastrelli ◽  
Emanuela Mazzon ◽  
Salvatore Cuzzocrea ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Water Soluble ◽  
Soluble Extract ◽  
Water Soluble Extract ◽  
Oxide Synthase ◽  
Inducible Nitric Oxide

In vivo pharmacological evaluation off two novel type II (inducible) nitric oxide synthase inhibitors

1995 ◽  
Vol 73 (5) ◽  
pp. 665-669 ◽  
Author(s):  
W. Ross Tracey ◽  
Masaki Nakane ◽  
Fatima Basha ◽  
George Carter
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
No Production ◽  
Type Ii ◽  
Nos Inhibitors ◽  
Oxide Synthase ◽  
Dose Dependent ◽  
Inducible Nitric Oxide

Selective type II (inducible) nitric oxide synthase (NOS) inhibitors have several potential therapeutic applications, including treatment of sepsis, diabetes, and autoimmune diseases. The ability of two novel, selective inhibitors of type II NOS, S-ethylisothiourea (EIT) and 2-amino-5,6-dihydro-6-methyl-4H-1,3-thiazine (AMT), to inhibit type II NOS function in vivo was studied in lipopolysaccharide (LPS) treated rats. Type II NOS activity was assessed by measuring changes in plasma nitrite and nitrate concentrations ([NOx]). Both EIT and AMT elicited a dose-dependent and >95% inhibition of the LPS-induced increase in plasma [NOx]. The ED50 values for EIT and AMT were 0.4 and 0.2 mg/kg, respectively. In addition, the administration of LPS and either NOS inhibitor resulted in a dose-dependent increase in animal mortality; neither compound was lethal when administered alone. Pretreatment with L-arginine (but not D-arginine) prevented the mortality, while not affecting the type II NOS-dependent NO production, suggesting the toxicity may be due to inhibition of one of the other NOS isoforms (endothelial or neuronal). Thus, although EIT and AMT are potent inhibitors of type II NOS function in vivo, type II NOS inhibitors of even greater selectivity may need to be developed for therapeutic applications.Key words: nitric oxide, nitrite, nitrate, sepsis, lipopolysaccharide.

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