Immunomodulatory Activity of Low Molecular-Weight Peptides from Nibea japonica in RAW264.7 Cells via NF-κB Pathway

In this study, a low molecular-weight (Mw) peptide named NJP (<1 kDa), was purified from a protein hydrolysate of Nibea japonica by ultrafiltration, and its immunomodulatory effect on RAW264.7 cells was evaluated. The lactate dehydrogenase (LDH) and MTT assays were performed to explore the cytotoxicity of NJP. The results showed that NJP promoted cell proliferation and had no significant toxic effects on RAW264.7 cells. Moreover, the cells formed multiple pseudopodia indicating that they were in activated state. Further tests showed that NJP significantly promoted phagocytic capacity, and the secretion of proinflammatory cytokines tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β). It also increased the synthesis of nitric oxide (NO) by upregulating inducible nitric oxide synthase (iNOS) protein level. Flow cytometry revealed that NJP promoted cell cycle progression and increased the percentage of cells in G0/G1 phase. NJP promoted IκBα degradation, p65 and nuclear factor (NF)-κB activation and translocation by up-regulating IKKα/β protein expression. In conclusion, these results indicated that NJP exerts immunomodulatory effects on RAW264.7 cells through the NF-κB signaling pathway. Therefore, NJP can be incorporated in the production of functional foods or nutraceuticals.

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Anti-Inflammatory Effect of Simonsinol on Lipopolysaccharide Stimulated RAW264.7 Cells through Inactivation of NF-κB Signaling Pathway

Molecules ◽

10.3390/molecules25163573 ◽

2020 ◽

Vol 25 (16) ◽

pp. 3573

Author(s):

Lian-Chun Li ◽

Zheng-Hong Pan ◽

De-Sheng Ning ◽

Yu-Xia Fu

Keyword(s):

Nitric Oxide ◽

Signaling Pathway ◽

Morphological Changes ◽

Raw264.7 Cells ◽

Enzyme Linked Immunosorbent Assay ◽

Tnf Α ◽

Anti Inflammatory ◽

Factor Α ◽

Oxide Synthase ◽

Necrosis Factor

Simonsinol is a natural sesqui-neolignan firstly isolated from the bark of Illicium simonsii. In this study, the anti-inflammatory activity of simonsinol was investigated with a lipopolysaccharide (LPS)-stimulated murine macrophages RAW264.7 cells model. The results demonstrated that simonsinol could antagonize the effect of LPS on morphological changes of RAW264.7 cells, and decrease the production of nitric oxide (NO), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) in LPS-stimulated RAW264.7 cells, as determined by Griess assay and enzyme-linked immunosorbent assay (ELISA). Furthermore, simonsinol could downregulate transcription of inducible nitric oxide synthase (iNOS), TNF-α, and IL-6 as measured by reverse transcription polymerase chain reaction (RT-PCR), and inhibit phosphorylation of the alpha inhibitor of NF-κB (IκBα) as assayed by Western blot. In conclusion, these data demonstrate that simonsinol could inhibit inflammation response in LPS-stimulated RAW264.7 cells through the inactivation of the nuclear transcription factor kappa-B (NF-κB) signaling pathway.

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14 EMF: Human Recombinant Low Molecular Weight Fibroblast Growth Factor 2 Protects the Heart From Reperfusion Injury Through Activation of FGF Receptors and Nitric Oxide Signaling

Annals of Emergency Medicine ◽

10.1016/j.annemergmed.2010.06.040 ◽

2010 ◽

Vol 56 (3) ◽

pp. S5 ◽

Cited By ~ 2

Author(s):

S.L. House ◽

G. Newman ◽

J.J. Schultz

Keyword(s):

Nitric Oxide ◽

Molecular Weight ◽

Growth Factor ◽

Reperfusion Injury ◽

Fibroblast Growth Factor ◽

Fibroblast Growth Factor 2 ◽

Low Molecular Weight ◽

Fibroblast Growth ◽

Nitric Oxide Signaling

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S-nitroso-albumin carries a thiol-labile pool of nitric oxide, which causes venodilation in the rat

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01014.2004 ◽

2005 ◽

Vol 289 (2) ◽

pp. H916-H923 ◽

Cited By ~ 11

Author(s):

Nelson N. Orie ◽

Patrick Vallance ◽

Dean P. Jones ◽

Kevin P. Moore

Keyword(s):

Nitric Oxide ◽

Molecular Weight ◽

Blood Flow ◽

Vascular Function ◽

Low Molecular Weight ◽

Aortic Blood Flow ◽

Hemodynamic Effects ◽

Rapid Decomposition ◽

Aortic Blood

It is now established that S-nitroso-albumin (SNO-albumin) circulates at low nanomolar concentrations under physiological conditions, but concentrations may increase to micromolar levels during disease states (e.g., cirrhosis or endotoxemia). This study tested the hypothesis that high concentrations of SNO-albumin observed in some diseases modulate vascular function and that it acts as a stable reservoir of nitric oxide (NO), releasing this molecule when the concentrations of low-molecular-weight thiols are increased. SNO-albumin was infused into rats to increase the plasma concentration from <50 nmol/l to ∼4 μmol/l. This caused a 29 ± 6% drop in blood pressure, 20 ± 4% decrease in aortic blood flow, and a 25 ± 14% reduction of renal blood flow within 10 min. These observations were in striking contrast to those of an infused arterial vasodilator (hydralazine), which increased aortic blood flow, and suggested that SNO-albumin acts primarily as a venodilator in vivo. This was confirmed by the observations that glyceryl trinitrate (a venodilator) led to similar hemodynamic changes and that the hemodynamic effects of SNO-albumin are reversed by infusion of colloid. Infusion of N-acetylcysteine into animals with artificially elevated plasma SNO-albumin concentrations led to the rapid decomposition of SNO-albumin in vivo and reproduced the hemodynamic effects of SNO-albumin infusion. These data demonstrate that SNO-albumin acts primarily as a venodilator in vivo and represents a stable reservoir of NO that can release NO when the concentrations of low-molecular-weight thiols are elevated.

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