scholarly journals Neosaxitoxin Inhibits the Expression of Inflammation Markers of the M1 Phenotype in Macrophages

Marine Drugs ◽  
2020 ◽  
Vol 18 (6) ◽  
pp. 283
Author(s):  
M. Cecilia Montero ◽  
Miguel del Campo ◽  
M. Bono ◽  
M. Valeska Simon ◽  
Julia Guerrero ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Mediators ◽  
Activated Macrophages ◽  
Voltage Gated Sodium Channels ◽  
Tnf Α ◽  
M1 Phenotype ◽  
Polymerase Chain ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor

(1) Background: Neosaxitoxin (NeoSTX) has been used as a local anesthetic, but its anti-inflammatory effects have not been well defined. In the present study, we investigate the effects of NeoSTX on lipopolysaccharide (LPS)-activated macrophages. (2) Methods: Raw 264.7 and equine PBMC cells were incubated with or without 100 ng/mL LPS in the presence or absence of NeoSTX (1µM). The expression of inflammatory mediators was assessed: nitric oxide (NO) content using the Griess assay, TNF-α content using the ELISA assay, and mRNA of inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) using a real-time polymerase chain reaction. (3) Results: NeoSTX (1 μM) significantly inhibited the release of NO, TNF-α, and expression of iNOS, IL-1β, and TNF-α in LPS-activated macrophages of both species studied. Furthermore, our study shows that the LPS-induced release of inflammatory mediators was suppressed by NeoSTX. Additionally, NeoSTX deactivated polarized macrophages to M1 by LPS without compromising its polarization towards M2. (4) Conclusions: NeoSTX inhibits LPS-induced release of inflammatory mediators from macrophages, and these effects may be mediated by the blockade of voltage-gated sodium channels (VGSC).

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

Molecules ◽  
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.

scholarly journals Bioactive Diterpenes, Norditerpenes, and Sesquiterpenes from a Formosan Soft Coral Cespitularia sp.

2021 ◽  
Vol 14 (12) ◽  
pp. 1252
Author(s):  
You-Cheng Lin ◽  
Chi-Chien Lin ◽  
Yi-Chia Chu ◽  
Chung-Wei Fu ◽  
Jyh-Horng Sheu
Keyword(s):  
Nitric Oxide ◽  
Soft Coral ◽  
2D Nmr ◽  
Inflammatory Protein ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor ◽  
Inducible Nitric Oxide

Chemical investigation of the soft coral Cespitularia sp. led to the discovery of twelve new verticillane-type diterpenes and norditerpenes: cespitulins H–O (1–8), one cyclic diterpenoidal amide cespitulactam L (9), norditerpenes cespitulin P (10), cespitulins Q and R (11 and 12), four new sesquiterpenes: cespilins A–C (13–15) and cespitulolide (16), along with twelve known metabolites. The structures of these metabolites were established by extensive spectroscopic analyses, including 2D NMR experiments. Anti-inflammatory effects of the isolated compounds were studied by evaluating the suppression of pro-inflammatory protein tumor necrosis factor-α (TNF-α) and nitric oxide (NO) overproduction, and the inhibition of the gene expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), in lipopolysaccharide-induced dendritic cells. A number of these metabolites were found to exhibit promising anti-inflammatory activities.

scholarly journals Protective effects of active hexose correlated compound in a rat model of liver injury after hepatectomy

2016 ◽  
Vol 6 (11) ◽  
pp. 702 ◽  
Author(s):  
Richi Nakatake ◽  
Yoshito Tanaka ◽  
Yosuke Ueyama ◽  
Hirokazu Miki ◽  
Morihiko Ishizaki ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Liver Injury ◽  
Rat Model ◽  
Inflammatory Mediators ◽  
Nuclear Factor ◽  
Protective Effects ◽  
Tnf Α ◽  
Oxide Synthase ◽  
Necrosis Factor ◽  
Inducible Nitric Oxide

Background: Recent evidence has indicated that a functional food, active hexose correlated compound (AHCC), has liver-protective effects via suppression of inflammatory mediators, such as inducible nitric oxide synthase (iNOS) and tumor necrosis factor (TNF)-α.Objective: This study aimed to investigate whether AHCC has beneficial effects in a rat model of endotoxin-induced liver injury after partial hepatectomy, in addition to clarifying the mechanisms of action of AHCC.Methods: Rats were treated with 70% of partial hepatectomy and lipopolysaccharide (PH/LPS) to induce acute liver injury. A normal diet with or without 2% AHCC was administered orally 10 days before 70% hepatectomy. Inflammatory mediators were analyzed.Results: AHCC improved the survival rate by 70% in PH/LPS rats. AHCC prevented an increase in serum transaminase levels, and histopathological changes and apoptosis in the liver. AHCC reduced iNOS mRNA and protein expression in the liver, resulting in inhibition of nitric oxide production. AHCC also reduced TNF-α, cytokine-induced neutrophil chemoattractant-1, and interleukin-6 mRNA expression, but enhanced expression of interleukin-10. An electrophoretic mobility shift assay with hepatic nuclear extracts demonstrated that AHCC reduced the activation of nuclear factor (NF)-κB induced by PH/LPS treatment.Conclusion: AHCC inhibits induction of inflammatory mediators, including iNOS and TNF-α, in part through inhibition of NF-κB activation in a rat model of liver injury. Our findings suggest that AHCC prevents postoperative liver failure after liver resection.Keywords: active hexose correlated compound, inducible nitric oxide synthase, liver injury, nuclear factor-κB, tumor necrosis factor-α

Surfactant protein A enhances mycobacterial killing by rat macrophages through a nitric oxide-dependent pathway

2000 ◽  
Vol 279 (2) ◽  
pp. L216-L223 ◽  
Author(s):  
Laura F. Weikert ◽  
Joseph P. Lopez ◽  
Rasul Abdolrasulnia ◽  
Zissis C. Chroneos ◽  
Virginia L. Shepherd
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Mediators ◽  
Protein A ◽  
Surfactant Protein ◽  
Nitric Oxide Production ◽  
Oxide Production ◽  
Tnf Α ◽  
Presence And Absence ◽  
Factor Α ◽  
Oxide Synthase

Surfactant-associated protein A (SP-A) is involved in surfactant homeostasis and host defense in the lung. We have previously demonstrated that SP-A specifically binds to and enhances the ingestion of bacillus Calmette-Guerin (BCG) organisms by macrophages. In the current study, we investigated the effect of SP-A on the generation of inflammatory mediators induced by BCG and the subsequent fate of ingested BCG organisms. Rat macrophages were incubated with BCG in the presence and absence of SP-A. Noningested BCG organisms were removed, and the release of tumor necrosis factor-α (TNF-α) and nitric oxide were measured at varying times. TNF-α and nitric oxide production induced by BCG were enhanced by SP-A. In addition, SP-A enhanced the BCG-induced increase in the level of inducible nitric oxide synthase protein. Addition of antibodies directed against SPR210, a specific macrophage SP-A receptor, inhibited the SP-A-enhanced mediator production. BCG in the absence of SP-A showed increased growth over a 5-day period, whereas inclusion of SP-A dramatically inhibited BCG growth. Inhibition of nitric oxide production blocked BCG killing in the presence and absence of SP-A. These results demonstrate that ingestion of SP-A-BCG complexes by rat macrophages leads to production of inflammatory mediators and increased mycobacterial killing.

Arginase 1 is expressed in myelocytes/metamyelocytes and localized in gelatinase granules of human neutrophils

Blood ◽  
2006 ◽  
Vol 109 (7) ◽  
pp. 3084-3087 ◽  
Author(s):  
Lars C. Jacobsen ◽  
Kim Theilgaard-Mönch ◽  
Erik I. Christensen ◽  
Niels Borregaard
Keyword(s):  
Nitric Oxide ◽  
Immune Responses ◽  
Tissue Regeneration ◽  
Human Neutrophils ◽  
Arginase 1 ◽  
Tnf Α ◽  
Activated Neutrophils ◽  
Factor Α ◽  
Oxide Synthase ◽  
Extracellular Environment

Abstract Arginase 1 (ARG1) metabolizes arginine, thus reducing the availability of arginine as a substrate for nitric oxide synthase (NOS). The decreased production of nitric oxide (NO) by NOS and the production of ornithine by ARG1 affect immune responses and tissue regeneration at sites of infection, respectively. We here demonstrate that ARG1 is synthesized in myelocytes/metamyelocytes and is stored in gelatinase granules. In accordance with this, activated neutrophils coreleased ARG1 and gelatinase to the extracellular environment on stimulation with phorbol-12-myristate 13-acetate (PMA), formyl-methionyl-leucyl-phenylalanine (fMLP), or tumor necrosis factor α (TNF-α). Overall, these findings define ARG1 as a genuine gelatinase granule protein and support a model in which activated neutrophils release ARG1 at sites of infection to modulate immune responses and promote tissue regeneration.

scholarly journals Alimentary induced fatty liver and adjuvant therapy with effective natural bioactive molecules

2011 ◽  
Vol 152 (26) ◽  
pp. 1035-1042 ◽  
Author(s):  
Viktor Hegedüs ◽  
Domokos Gerő ◽  
Zoltán Mihály ◽  
Attila Szijártó ◽  
Tivadar Zelles ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Fatty Liver ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Redox Homeostasis ◽  
Mrna Levels ◽  
Factor Α ◽  
Oxide Synthase ◽  
Necrosis Factor ◽  
Inducible Nitric Oxide

Changes of redox-homeostasis generate cytokines, and free radicals influence many intracellular signaling pathways in different liver diseases. Liophylised table beet and carrot powder (GPS Powder Kft. 1361/004/2003BFÁÉÉÁ) containing bioactive components such as betaine, betanins, betaxanthins, flavonoids, polyphenols, glutamine, beta carotene, vitamins and folic acid may produce changes various cellular pathways. Aim: The aim of this study was to determine the protecting effects of bioactive agents of the liophylised table beet and carrot powder on fatty liver in a “short term” experiment. Method: Male Wistar rats were fed with chow with or without high fat (2% cholesterol, 0.5% cholic acid, 20% sunflower oil) and treated with 0.1 or 1 g/bwkg/day natural product for ten days parallel with the feedings. Cyclooxygenase-2, inducible nitric oxide synthase and tumor necrosis factor-α mRNA levels were determined using molecular biologic methods. Free radicals, H-donating activity, reducing power and free SH-group concentrations were determined by luminometry and spectrophotometry. Mobilized methyl groups were assayed by over pressure liquid chromatography method in liver homogenates. Results: It was found that the higher dose of the natural product better decreased the induced free radical reactions, cyclooxygenase-2, inducible nitric oxide synthase and tumor necrosis factor-α mRNA-levels both in normal and fatty liver tissues. Although treatments failed to exert significant changes in all global antioxidant parameters, mobilized methyl group concentrations were higher after treatments in fatty liver. Favorable tendencies were also noted in the redox-homeostasis of the fatty liver after treatment. Conclusions: As expected, lyophylised table beet and carrot proved to be a “functional food” in rats with alimentary fat induced fatty liver. It cannot be ruled out that this beneficial effect may have clinical relevance. Orv. Hetil., 2011, 152, 1035–1042.

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