scholarly journals DDAH1 SNP rs480414 that protects against the development of pulmonary hypertension in bronchopulmonary dysplasia results in lower nitric oxide production in neonatal cord blood-derived lymphoblastoid cell lines

2021 ◽  
pp. 1-9
Author(s):  
Avante D. Milton ◽  
Hanadi Almazroue ◽  
Yi Jin ◽  
Gloria Zender ◽  
Jennifer K. Trittmann
Keyword(s):  
Nitric Oxide ◽  
Pulmonary Hypertension ◽  
Cord Blood ◽  
Mrna Expression ◽  
Cell Lines ◽  
Bronchopulmonary Dysplasia ◽  
Caspase 3 ◽  
Inos Mrna ◽  
No Production ◽  
Lymphoblastoid Cell Lines

BACKGROUND: Bronchopulmonary dysplasia (BPD) is chronic lung disease of prematurity and pulmonary hypertension (PH) is a major contributor to morbidity and mortality in BPD patients. Nitric oxide (NO) is a vasodilator and apoptotic mediator made by NO synthase (NOS). NOS is inhibited by asymmetric dimethylarginine (ADMA), and dimethylarginine dimethylaminohydrolase (DDAH) hydrolyzes ADMA. Previously, in a BPD patient cohort, we identified single nucleotide polymorphism (SNP) DDAH1 rs480414 (G >  A) that was protective against developing PH. This study aims to determine functional consequences of the DDAH1 SNP in lymphoblastoid cell lines (LCLs) derived from neonatal cord blood. We tested the hypothesis that DDAH1 SNP (AA) results in DDAH1 gain of function, leading to greater NO-mediated apoptosis compared to DDAH1 wild-type (GG) in LCLs. METHODS: LCLs were analyzed by Western blot (DDAH1, cleaved and total caspase-3 and -8, and β-actin), and RT-PCR (DDAH1, iNOS). Cell media assayed for nitrites with chemiluminescence NO analyzer, and conversion of ADMA to L-citrulline was measured by spectrophotometry. RESULTS: LCLs with DDAH1 SNP had similar levels of DDAH1 protein and mRNA expression, as well as DDAH activity, compared to DDAH1 WT LCLs. There were also no changes in cleaved caspase-3 and -8 protein levels. LCLs with DDAH1 SNP had similar iNOS mRNA expression. Nitrite levels in media were lower for DDAH1 SNP LCLs compared to DDAH1 WT LCLs (p <  0.05). CONCLUSION: Contrary to our hypothesis, we found that NO production was lower in DDAH1 SNP LCLs, indicative of a loss of function phenotype.

Involvement of nitric oxide in farnesyltransferase inhibitor–mediated apoptosis in chronic myeloid leukemia cells

Blood ◽  
2003 ◽  
Vol 102 (4) ◽  
pp. 1490-1498 ◽  
Author(s):  
Carmine Selleri ◽  
Jaroslaw P. Maciejewski ◽  
Nunzia Montuori ◽  
Patrizia Ricci ◽  
Valeria Visconte ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Chronic Myeloid Leukemia ◽  
Myeloid Leukemia ◽  
Caspase 3 ◽  
Inos Mrna ◽  
No Production ◽  
Farnesyltransferase Inhibitors ◽  
Fasl Expression ◽  
Cytotoxic Effects ◽  
Marrow Cells

Abstract The mechanism of action of farnesyltransferase inhibitors (FTIs) has not been fully clarified. We investigated the cytotoxic effects of various FTIs in chronic myeloid leukemia (CML), using LAMA cells and marrow cells from 40 CML patients in chronic phase. FTI-mediated cytotoxic effect was observed in LAMA cells and in 65% of primary CML cells, whereas marrow cells from controls were only weakly affected. Cytotoxic effects were partially related to enhanced apoptosis; however, Fas-receptor (FasR) and Fas-ligand (FasL) expression were not modified by FTIs. Susceptibility to FTI-mediated inhibition did not correlate with FasR/FasL expression in CD34+ CML cells. Moreover, intra-cellular activation of caspase-1 and -8 were not altered by FTIs, and their blockade did not reverse FTI toxicity. However, we observed FTI-induced activation of caspase-3, and its inhibition partially reverted FTI-induced apoptosis. FTIs did not modulate bcl2, bclxL, and bclxS expression, whereas they increased inducible nitric oxide (iNOS) mRNA and protein levels, resulting in higher NO production. Furthermore, C3 exoenzyme, a Rho inhibitor, significantly increased iNOS expression in CML cells, suggesting that FTIs may up-regulate NO formation at least partially through FTI-mediated inhibition of Rho. We conclude that FTIs induce selective apoptosis in CML cells via activation of iNOS and caspase-3.

Enhanced Expression of Inducible Nitric Oxide Synthase by Juzen-Taiho-To in LPS-Activated RAW264.7 Cells, a Murine Macrophage Cell Line

2000 ◽  
Vol 28 (02) ◽  
pp. 217-226 ◽  
Author(s):  
Hiroshi Kawamata ◽  
Hiroshi Ochiai ◽  
Naoki Mantani ◽  
Katsutoshi Terasawa
Keyword(s):  
Nitric Oxide ◽  
Mrna Expression ◽  
Cell Line ◽  
Raw264.7 Cells ◽  
Inos Mrna ◽  
No Production ◽  
Murine Macrophage ◽  
Macrophage Cell Line ◽  
Macrophage Cell ◽  
Murine Macrophage Cell Line

We have investigated the effect of Juzen-taiho-to (TJ-48) on inducible NO synthase (iNOS) expression and nitric oxide (NO) production in RAW264.7 cells, a murine macrophage cell line. TJ-48-lipopolysaccharide (LPS) combination induced iNOS mRNA expression earlier, stronger and remained longer that paralleled but with a higher NO production compared to LPS stimulation. TJ-48 itself showed no inducible effect either no NO production or iNOS mRNA expression. This phenomenon could be considered to contribute, at least in part, to the beneficial effects of TJ-48 through the iNOS-mediated activation of biodefense mechanism.

scholarly journals Suppressive Effect of Quercetin on Nitric Oxide Production from Nasal Epithelial Cells In Vitro

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Nachi Ebihara ◽  
Kana Takahashi ◽  
Haruka Takemura ◽  
Yuko Akanuma ◽  
Kazuhito Asano ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Epithelial Cells ◽  
Mrna Expression ◽  
Suppressive Effect ◽  
Inos Mrna ◽  
No Production ◽  
Minimum Concentration ◽  
Nasal Epithelial Cells ◽  
Human Nasal Epithelial Cells

Nitric oxide (NO) is known to play pivotal roles as one of the final effector molecules in the development of allergic diseases, including allergic rhinitis (AR). Although quercetin has been reported to attenuate the clinical conditions of AR, its influence on NO production is not well defined. The present study aimed to examine the influence of quercetin on in vitro NO production from nasal epithelial cells after interleukin- (IL-) 4 stimulation. Human nasal epithelial cells (HNEpCs) at a concentration of 1 x 105 cells/ml were stimulated with 10.0 ng/ml of IL-4 in the presence and absence of quercetin. After 48 hours, the culture supernatants were collected and assayed for NO (NO2 and NO3) using the Griess method. The influences of quercetin on the transcription factor, STAT6, activation, and iNOS mRNA expression were also examined using ELISA and real-time quantitative RT-PCR, respectively. Addition of quercetin to cell cultures caused suppression of NO production from HNEpCs after IL-4 stimulation. The minimum concentration of quercetin that caused significant suppression was 1.0 nM. Treatment of cells with quercetin at more than 1.0 nM suppressed STAT6 activation and iNOS mRNA expression induced by IL-4 stimulation. The present results strongly suggested that quercetin favorably modified the clinical condition of AR through the suppression of NO production from nasal epithelial cells after IL-4 stimulation.

scholarly journals Effect of mast cell granules on the gene expression of nitric oxide synthase and tumour necrosis factor-α in macrophages

1998 ◽  
Vol 7 (5) ◽  
pp. 355-361 ◽  
Author(s):  
Y. Li ◽  
T. D. Nguyen ◽  
A. C. Stechschulte ◽  
D. J. Stechschulte ◽  
K. N. Dileepan
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Mast Cell ◽  
Nitric Oxide Synthase ◽  
Mrna Expression ◽  
Inos Mrna ◽  
No Production ◽  
Activated Macrophages ◽  
Factor Α ◽  
Oxide Synthase

Previous studies have shown that mast cell granules (MCG) inhibit numerous macrophage functions including tumour cytotoxicity, superoxide and nitric oxide (NO) production, and FCγ2a receptor-mediated phagocytosis. In this study, the effect of MCG on macrophage TNFα and nitric oxide synthase (iNOS) mRNA expression, and the production and fate of TNFα were examined. Upon activation with LPS+IFNγ, macrophages expressed both TNFα and iNOS mRNA and produced both TNFα and NO. Co-incubation of LPS+IFNγ-activated macrophages with MCG resulted in dose-dependent inhibition of iNOS mRNA expression. TNFα production in the activated macrophages was decreased by MCG, which was associated with a reduction in TNFα mRNA expression. MCG were also capable of degrading both macrophage-generated and recombinant TNFα. The direct effect of MCG on TNFα was partially reversed by a mixture of protease inhibitors. These results demonstrate that MCG decrease the production of NO and TNFα by inhibiting macrophage iNOS and TNFα gene expression. Furthermore, MCG post-transcriptionally alter TNFα levels via proteolytic degradation.

Tissue Characterization of Hypoxia, Nitric Oxide and Apoptosis Pathways in a Baboon Model of E. coli Sepsis.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 138-138
Author(s):  
Lacramioara Ivanciu ◽  
Oana Herlea ◽  
Hua Zhu ◽  
Fletcher B. Taylor ◽  
Cristina Lupu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Lymph Nodes ◽  
Mrna Expression ◽  
Organ Failure ◽  
Caspase 3 ◽  
No Production ◽  
E Coli ◽  
Peritubular Capillaries ◽  
Apoptosis Pathways ◽  
Spleen And Lymph Nodes

Abstract Sepsis - the most common cause of death in hospitalized patients -is characterized by severe inflammatory response and profound systemic vasculitic pathology accompanied by activation of blood coagulation. We observed previously that infusion of E. coli in baboons produced severe disruption of the microcirculation, such as capillary leakage, intravascular coagulation and tissue injury, which may lead to global tissue hypoxia, shock, organ failure, and death. Here, we report data on the temporal dynamics of tissue specific changes of hypoxia, nitric oxide (NO) and apoptosis pathways in response to sublethal or lethal E. coli challenge. Animals were administered sublethal doses of E. coli (LD30–50; 108 CFU/kg) and sacrificed after 2, 8 and 24 hours or lethal doses (LD100; 9x109 −1x1010 CFU/kg) for 8 hours. Both groups were compared to non challenged controls (n=3 per experimental condition). Six organs (lung, liver, heart, kidney, spleen and lymph nodes) were analyzed by immunofluorescence/confocal imaging for Hypoxia Inducible Factor 1 (HIF1α), NOS2, NOS3 nitrotyrosine (NT), inflammatory cell markers (myeloperoxidase and CD68 for neutrophils and macrophages, respectively), and apoptosis markers (active caspase-3, TUNEL, Bcl2, Bax). Tissue extracts were analyzed by ELISA (NT and caspase-3), dot and western blot (NT, Bcl2 and Bax) and RT-PCR and microarray assays for mRNA expression. The results show that HIF1α mRNA was increased by 2–3 fold, reaching maximum values at 2 hours in the lung and 24 hours in the liver. HIF1α nuclear translocation was detected by immunostaining at 8 hours in lung and 24 hours in the liver, especially in the LD100 E. coli challenged baboons. HIF1α functions as a master transcriptional regulator of the adaptive response to hypoxia, and controls the expression of over 40 genes including NOS2, an inducible enzyme that induces NO production and thus decreases the vascular tone, and VEGF, a very potent permeability factor. NOS2 mRNA and protein were induced after 8 hours mainly in inflammatory cells, while endothelial NOS3 showed a transient decrease at 2–8 hours, and increased at 24 hours as compared to controls. The overall increase in NO production was reflected in transient high levels of nitrosylated proteins at 8 hours in sublethal animals and persistent high levels in lethal baboons. Ultrastructural analysis of lung and kidney performed by electron microscopy showed signs of defective permeability, such as accumulation of plasma proteins in the lung alveolae and in the subendothelium of the kidney peritubular capillaries, concomitant with intra- and/or extravascular fibrin deposition. Dose-dependent induction of apoptosis was detected by TUNEL and caspase-3 staining, especially in the proximal contort tubes of the kidney, hepatocytes, lymphoid and pericapsular cells of spleen and lymph nodes. Mitochondrial manganese superoxide dismutase (SOD2), a protective enzyme produced in reaction to oxidative stress had a latter response, reaching the maximum mRNA expression at 8 hour in lung and 24 hours in the liver. Taken together, these results place hypoxia as a key factor in the development of organ dysfunction and multiple organ failure in sepsis and suggest that targeting hypoxia controlled transcription factors, such as HIF1α, or upregulating the antioxidant mechanisms may represent valuable therapeutic approaches.

scholarly journals Induction of nitric oxide synthase by rotavirus enterotoxin NSP4: implication for rotavirus pathogenicity

2007 ◽  
Vol 88 (7) ◽  
pp. 2064-2072 ◽  
Author(s):  
Mohamed A. Borghan ◽  
Yoshio Mori ◽  
Abu-Baker El-Mahmoudy ◽  
Naoto Ito ◽  
Makoto Sugiyama ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mrna Expression ◽  
Ex Vivo ◽  
Inos Expression ◽  
Intestinal Cells ◽  
Inos Mrna ◽  
No Production ◽  
Post Inoculation ◽  
Structural Protein ◽  
Rotavirus Infection

Rotavirus non-structural protein (NSP) 4 can induce aqueous secretion in the gastrointestinal tract of neonatal mice through activation of an age- and Ca2+-dependent plasma membrane anion permeability. Accumulating evidence suggests that nitric oxide (NO) plays a role in the modulation of aqueous secretion and the barrier function of intestinal cells. This study investigated transcriptional changes in inducible NO synthase (iNOS), an enzyme responsible for NO production, after rotavirus infection in mice and after treatment of intestinal cells with NSP4. Diarrhoea was observed in 5-day-old CD-1 mice from days 1 to 3 after inoculation with 107 focus-forming units of different rotavirus strains. Ileal iNOS mRNA expression was induced as early as 6 h post-inoculation, before the onset of clinical diarrhoea in infected mice, and was upregulated during the course of rotavirus-induced diarrhoea. Ex vivo treatment of ilea excised from CD-1 suckling mice with NSP4 resulted in upregulation of ileal iNOS mRNA expression within 4 h. Furthermore, NSP4 was able to induce iNOS expression and NO production in murine peritoneal macrophages and RAW264.7 cells. The specificity of NSP4 inducibility was confirmed by the inhibitory effect of anti-NSP4 serum. Using a series of truncated NSP4s, the domain responsible for iNOS induction in macrophages was mapped to the reported enterotoxin domain, aa 109–135. Thus, rotavirus infection induces ileal iNOS expression in vivo and rotavirus NSP4 also induces iNOS expression in the ileum and macrophages. Together, these findings suggest that NO plays a role in rotavirus-induced diarrhoea.

scholarly journals Cord blood-derived endothelial colony-forming cell function is disrupted in congenital diaphragmatic hernia

2016 ◽  
Vol 310 (11) ◽  
pp. L1143-L1154 ◽  
Author(s):  
Hideshi Fujinaga ◽  
Hiroko Fujinaga ◽  
Nobuyuki Watanabe ◽  
Tomoko Kato ◽  
Moe Tamano ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Congenital Diaphragmatic Hernia ◽  
Cord Blood ◽  
Mrna Expression ◽  
Diaphragmatic Hernia ◽  
Cell Function ◽  
De Novo ◽  
Normal Lung ◽  
No Production

Vascular growth is necessary for normal lung development. Although endothelial progenitor cells (EPCs) play an important role in vascularization, little is known about EPC function in congenital diaphragmatic hernia (CDH), a severe neonatal condition that is associated with pulmonary hypoplasia. We hypothesized that the function of endothelial colony-forming cells (ECFCs), a type of EPC, is impaired in CDH. Cord blood (CB) was collected from full-term CDH patients and healthy controls. We assessed CB progenitor cell populations as well as plasma vascular endothelial growth factor (VEGF) and stromal cell-derived factor 1α (SDF1α) levels. CB ECFC clonogenicity; growth kinetics; migration; production of VEGF, SDF1α, and nitric oxide (NO); vasculogenic capacity; and mRNA expression of VEGF-A, fms-related tyrosine kinase 1 (FLT1), kinase insert domain receptor (KDR), nitric oxide synthase (NOS) 1–3, SDF1, and chemokine (C-X-C motif) receptor 4 (CXCR4) were also assessed. Compared with controls, CB ECFCs were decreased in CDH. CDH ECFCs had reduced potential for self-renewal, clonogenicity, proliferation, and migration. Their capacity for NO production was enhanced but their response to VEGF was blunted in CDH ECFCs. In vivo potential for de novo vasculogenesis was reduced in CDH ECFCs. There was no difference in CB plasma VEGF and SDF1α concentrations, VEGF and SDF1α production by ECFCs, and ECFC mRNA expression of VEGF-A, FLT1, KDR, NOS1-3, SDF1, and CXCR4 between CDH and control subjects. In conclusion, CB ECFC function is disrupted in CDH, but these changes may be caused by mechanisms other than alteration of VEGF-NO and SDF1-CXCR4 signaling.

scholarly journals Comparing the protective effects of resveratrol, curcumin and sulforaphane against LPS/IFN-γ-mediated inflammation in doxorubicin-treated macrophages

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Haidy A. Saleh ◽  
Eman Ramdan ◽  
Mohey M. Elmazar ◽  
Hassan M. E. Azzazy ◽  
Anwar Abdelnaser
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Response ◽  
Raw 264.7 Cells ◽  
Inos Mrna ◽  
No Production ◽  
Raw 264.7 ◽  
Mrna Levels ◽  
Protective Effects ◽  
Tnf Α ◽  
Ifn Γ

AbstractDoxorubicin (DOX) chemotherapy is associated with the release of inflammatory cytokines from macrophages. This has been suggested to be, in part, due to DOX-mediated leakage of endotoxins from gut microflora, which activate Toll-like receptor 4 (TLR4) signaling in macrophages, causing severe inflammation. However, the direct function of DOX on macrophages is still unknown. In the present study, we tested the hypothesis that DOX alone is incapable of stimulating inflammatory response in macrophages. Then, we compared the anti-inflammatory effects of curcumin (CUR), resveratrol (RES) and sulforaphane (SFN) against lipopolysaccharide/interferon-gamma (LPS/IFN-γ)-mediated inflammation in the absence or presence of DOX. For this purpose, RAW 264.7 cells were stimulated with LPS/IFN-γ (10 ng/mL/10 U/mL) in the absence or presence of DOX (0.1 µM). Our results showed that DOX alone is incapable of stimulating an inflammatory response in RAW 264.7 macrophages. Furthermore, after 24 h of incubation with LPS/IFN-γ, a significant increase in tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and inducible nitric oxide synthase (iNOS) mRNA levels was observed. Similarly, nitric oxide (NO) production and TNF-α and IL-6 protein levels were significantly upregulated. Moreover, in LPS/IFN-γ-treated macrophages, the microRNAs (miRNAs) miR-146a, miR-155, and miR-21 were significantly overexpressed. Interestingly, upon testing CUR, RES, and SFN against LPS/IFN-γ-mediated inflammation, only SFN was able to significantly reverse the LPS/IFN-γ-mediated induction of iNOS, TNF-α and IL-6 and attenuate miR-146a and miR-155 levels. In conclusion, SFN, at the transcriptional and posttranscriptional levels, exhibits potent immunomodulatory action against LPS/IFN-γ-stimulated macrophages, which may indicate SFN as a potential treatment for DOX-associated inflammation.

Cytokine and inflammatory mediators are associated with cytotoxic, anti-inflammatory and apoptotic activity of honeybee venom

2020 ◽  
Vol 0 (0) ◽  
Author(s):  
Mohamed A. Salama ◽  
Mohamed A. Younis ◽  
Roba M. Talaat
Keyword(s):  
Nitric Oxide ◽  
Cell Lines ◽  
Cancer Cell ◽  
Hela Cells ◽  
No Production ◽  
Hep G2 ◽  
Normal Cells ◽  
Tnf Α ◽  
Ifn Γ ◽  
Mcf 7

AbstractObjectiveThe present study aimed to evaluate cytotoxic, apoptotic, and anti-inflammatory properties of bee venom (BV) as well as changes in cytokine secretion levels and nitric oxide (NO) production using three different cancer cell lines [liver (Hep-G2), breast (MCF-7), and cervical (HPV-18 infected HeLa cells)] and two normal cells (splenocytes and macrophages (MQ).MethodsCytotoxic activity of BV against tumor cell lines and normal splenocytes/MQ was tested by MTT assay. By ELISA (ELISA); Tumor necrosis factor (TNF-α), Interleukine (IL-10) and interferon (IFN-γ) were measured. Caspase three expressions was evaluated using reverse transcription-polymerase chain reaction (RT-PCR). Nitric oxide (NO) was estimated using a colorimetric assay.ResultsBV has a significant cytotoxic effect on all cell lines in a dose- and time-dependent manner; none of them was toxic for normal cells. Treating Hep-G2 cells with BV showed a reduction in IL-10, elevation in TNF-α with no change in IFN-γ level. MCF-7 cells have low IL-10 and TNF-α and high IFN-γ production level. Elevation of IL-10 and IFN-γ coincides with a reduction in TNF-α level was demonstrated in HeLa cells. The expression of Caspase three was dramatically increased with elevation in BV concentration in all tested cancer cell lines. A gradual decrease in NO production by MQ with increasing BV dose was observed.ConclusionTaken together, our results stressed on the importance of BV as a potent anti-tumor agent against various types of cancers (Liver, Breast, and Cervix). Further steps towards the use of BV for pharmacological purposes must be done.

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 &micro;g 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 &lt; 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 &lt; 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&nbsp;&lt; 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 &lt; 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.

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