scholarly journals Cnicin from Centaurea benedicta L. is an active compound against skin inflammation in a mouse model

2021 ◽  
Author(s):  
Orlando Vieira Sousa ◽  
Guilherme C. Gonçalves ◽  
Lucas S. Queiroz ◽  
Everton A. Ferreira ◽  
Bruna C. S. Santos ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Mouse Model ◽  
Skin Inflammation ◽  
Cyclooxygenase 1 ◽  
Tnf Α ◽  
Inflammatory Processes ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase

Abstract Centaurea benedicta L., commonly known as “cardo santo,” is used as a tonic, antidepressant, anti-inflammatory, antibacterial, and antiseptic in traditional medicine. This study evaluated the topical anti-inflammatory potential of an extract (ECB) and cnicin (CNI) from C. benedicta leaves in a mouse model. Activity was assessed using the ear edema method with croton oil, phenol, capsaicin, and histamine as phlogistic agents. Myeloperoxidase (MPO), N-acetyl-β-D-glucosaminidase (NAG), nitric oxide (NO), t umor necrosis factor α (TNF-α), interleukin 6 (IL-6), and histopathology were assessed as markers of edema/inflammation. Interaction profiles between CNI and cyclooxygenase-1 and -2, induced nitric oxide synthase, and glucocorticoid receptor were examined with molecular docking. Twenty-four h after induction of inflammation, ECB and CNI treatments decreased the thickness and weight of ears by 39.59%– 94.72%. MPO, NAG, NO, TNF-α, and IL-6 levels were also reduced. Histopathological, treatments reduced edema thickness, leukocytes, and vasodilation. Inflammation induced by phenol and histamine was inhibited by ECB and CNI, and ECB suppressed capsaicin-induced inflammation. CNI interacts with cyclooxygenase-1 and nitric oxide synthase through conventional hydrogen bonds, indicating inhibition of these enzymes. ECB and its compound cnicin reduce chemically-induced inflammation in mice suggesting new possibilities for the treatment of diseases associated with dermal inflammatory processes.

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 Phytosterols Suppress Phagocytosis and Inhibit Inflammatory Mediators via ERK Pathway on LPS-Triggered Inflammatory Responses in RAW264.7 Macrophages and the Correlation with Their Structure

Foods ◽  
2019 ◽  
Vol 8 (11) ◽  
pp. 582 ◽  
Author(s):  
Yuan ◽  
Zhang ◽  
Shen ◽  
Jia ◽  
Xie
Keyword(s):  
Nitric Oxide ◽  
Inflammatory Responses ◽  
Ester Group ◽  
No Production ◽  
Raw264.7 Macrophages ◽  
Extracellular Signal ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α ◽  
Oxide Synthase

Phytosterols, found in many commonly consumed foods, exhibit a broad range of physiological activities including anti-inflammatory effects. In this study, the anti-inflammatory effects of ergosterol, β-sitosterol, stigmasterol, campesterol, and ergosterol acetate were investigated in lipopolysaccharide (LPS)-induced RAW264.7 macrophages. Results showed that all phytosterol compounds alleviated the inflammatory reaction in LPS-induced macrophage models; cell phagocytosis, nitric oxide (NO) production, release of tumor necrosis factor-α (TNF-α), and expression and activity of pro-inflammatory mediator cyclooxygenase-2 (COX-2), inducible nitric oxide synthase (iNOS), and phosphorylated extracellular signal-regulated protein kinase (p-ERK) were all inhibited. The anti-inflammatory activity of β-sitosterol was higher than stigmasterol and campesterol, which suggests that phytosterols without a double bond on C-22 and with ethyl on C-24 were more effective. However, inconsistent results were observed upon comparison of ergosterol and ergosterol acetate (hydroxy or ester group on C-3), which suggest that additional research is still needed to ascertain the contribution of structure to their anti-inflammatory effects.

The role of neuronal NO synthase in the respiratory effects of TNF-α

2021 ◽  
Author(s):  
A.A. Klinnikova ◽  
G.A. Danilova ◽  
N.P. Aleksandrova
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Ventilatory Response ◽  
Neuronal Nitric Oxide Synthase ◽  
Key Words Cytokines ◽  
Respiratory Effects ◽  
Tnf Α ◽  
Before And After ◽  
Factor Α ◽  
Oxide Synthase

It was shown that an increase level of proinflammatory cytokines has a modulating effect on the reflex control of respiration. The aim of this study was to investigate the involvement of neuronal nitric oxide synthase (nNOS) in the mechanisms of the influence of an increased level of Tumor necrosis factor – α (TNF-α) on the hypoxic ventilatory response. To achieve this goal, experiments were carried out on urethane anesthetized rats with intravenous administration of TNF-α before and after pretreatment with 7-nitroindazole specific nNOS inhibitor. The hypoxic ventilation response was assessed by rebreathing with a hypoxic gas mixture before and after administration of TNF-α. We found that TNF-α decreased the ventilatory response to hypoxia. Pretreatment with nNOS inhibitor reduced respiratory effects of TNF-α. Key words: cytokines, TNF-α, hypoxia, chemoreflex, respiration, ventilation, neuronal nitric oxide synthase.

Antithrombin prevents endotoxin-induced hypotension by inhibiting the induction of nitric oxide synthase in rats

Blood ◽  
2002 ◽  
Vol 99 (5) ◽  
pp. 1638-1645 ◽  
Author(s):  
Hirotaka Isobe ◽  
Kenji Okajima ◽  
Mitsuhiro Uchiba ◽  
Naoaki Harada ◽  
Hiroaki Okabe
Keyword(s):  
Nitric Oxide ◽  
Septic Shock ◽  
Nitric Oxide Synthase ◽  
Messenger Rna ◽  
Inos Mrna ◽  
Therapeutic Effects ◽  
Induced Hypotension ◽  
Tnf Α ◽  
Factor Α ◽  
Oxide Synthase

Antithrombin (AT) prevents Escherichia coli–induced hypotension in animal models of sepsis, and it further reduces the mortality of patients with septic shock. In the present study, we examined whether AT may prevent the endotoxin (ET)-induced hypotension by promoting the endothelial release of prostacyclin (PGI2) in rats. Intravenous administration of AT (250 U/kg) prevented both hypotension and the increases in plasma levels of NO2−/NO3− in rats given ET. Lung expression of messenger RNA (mRNA) for tumor necrosis factor-α (TNF-α) was transiently increased after ET administration, followed by the increases in lung tissue levels of TNF-α. Both the lung activity of the inducible form of nitric oxide synthase (iNOS) and the lung expression of iNOS mRNA in animals administered ET were gradually increased after the TNF-α mRNA expression had peaked. Administration of AT significantly inhibited these increases. Neither DEGR-F.Xa, a selective inhibitor of thrombin generation, nor Trp49-modified AT, which is not capable of promoting the endothelial release of PGI2, showed any effects on these changes induced by ET. Administration of antirat TNF-α antibody produced effects similar to those induced by AT. Indomethacin pretreatment abrogated the effects induced by AT. Iloprost, a stable derivative of PGI2, produced effects similar to those of AT. These findings suggested that AT prevents the ET-induced hypotension by inhibiting the induction of iNOS through inhibiting TNF-α production. These effects of AT could be mediated by the promotion of endothelial release of PGI2 and might at least partly explain the therapeutic effects for septic shock.

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 gem-Difluorobisarylic derivatives: design, synthesis and anti-inflammatory effect

BMC Chemistry ◽  
2019 ◽  
Vol 13 (1) ◽  
Author(s):  
Abeer J. Ayoub ◽  
Layal Hariss ◽  
Nehme El-Hachem ◽  
Ghewa A. El-Achkar ◽  
Sandra E. Ghayad ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Protein Expression ◽  
Interleukin 6 ◽  
Cyclooxygenase 2 ◽  
Prostaglandin E ◽  
Diaryl Ethers ◽  
Cyclooxygenase 1 ◽  
Anti Inflammatory ◽  
Oxide Synthase

Abstract Introduction New fluorinated diaryl ethers and bisarylic ketones were designed and evaluated for their anti-inflammatory effects in primary macrophages. Methods The synthesis of the designed molecules started from easily accessible and versatile gem-difluoro propargylic derivatives. The desired aromatic systems were obtained using Diels–Alder/aromatization sequences and this was followed by Pd-catalyzed coupling reactions and, when required, final functionalization steps. Both direct inhibitory effects on cyclooxygenase-1 or -2 activities, protein expression of cyclooxygenase-2 and nitric oxide synthase-II and the production of prostaglandin E2, the pro-inflammatory nitric oxide and interleukin-6 were evaluated in primary murine bone marrow-derived macrophages in response to lipopolysaccharide. Docking of the designed molecules in cyclooxygenase-1 or -2 was performed. Results Only fluorinated compounds exerted anti-inflammatory activities by lowering the secretion of interleukin-6, nitric oxide, and prostaglandin E2, and decreasing the protein expression of inducible nitric oxide synthase and cyclooxygenase-2 in mouse primary macrophages exposed to lipopolysaccharide, as well as cyclooxygenase activity for some inhibitors with different efficiencies depending on the R-groups. Docking observation suggested an inhibitory role of cyclooxygenase-1 or -2 for compounds A3, A4 and A5 in addition to their capacity to inhibit nitrite, interleukin-6, and nitric oxide synthase-II and cyclooxygenase-2 expression. Conclusion The new fluorinated diaryl ethers and bisarylic ketones have anti-inflammatory effects in macrophages. These fluorinated compounds have improved potential anti-inflammatory properties due to the fluorine residues in the bioactive molecules.

scholarly journals Role of inducible nitric oxide synthase in the regulation of VCAM-1 expression in gut inflammation

1999 ◽  
Vol 277 (3) ◽  
pp. G572-G576 ◽  
Author(s):  
Shigeyuki Kawachi ◽  
Adam Cockrell ◽  
F. Stephen Laroux ◽  
Laura Gray ◽  
D. Neil Granger ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Wild Type ◽  
Chronic Colitis ◽  
Antibody Technique ◽  
Tnf Α ◽  
Factor Α ◽  
Oxide Synthase

The objectives of this study were to assess the role of the inducible isoform of nitric oxide synthase (iNOS) on vascular cell adhesion molecule 1 (VCAM-1) expression in vivo in an acute model of inflammation induced in iNOS-deficient (iNOS−/−) mice and compare these data to those obtained by pharmacological inhibition of iNOS in a CD4+ T lymphocyte-dependent model of chronic colitis. VCAM-1 expression was quantified in vivo using the dual radiolabel monoclonal antibody technique. We found that intraperitoneal injection of 10 μg/kg tumor necrosis factor-α (TNF-α) enhanced VCAM-1 expression by approximately twofold in the colon, cecum, and stomach but not small intestine in iNOS−/−mice compared with TNF-α-injected wild-type mice. Injection of wild-type mice with 25 μg/kg TNF-α further enhanced VCAM-1 expression by approximately twofold compared with wild-type mice injected with 10 μg/kg TNF-α; however, VCAM-1 expression was not further enhanced in any gastrointestinal organ system in iNOS−/− mice. In a second series of experiments, we found that continuous inhibition of iNOS using oral administration of N G-iminoethyl-l-lysine did not alter the enhanced levels of VCAM-1 expression in the colon nor did it alter the severity of colonic inflammation in SCID mice reconstituted with CD4+, CD45RBhigh T cells. We conclude that iNOS may regulate VCAM-1 expression in acute inflammation; however, this effect is modest and tissue specific and occurs only when VCAM-1 expression is submaximal. iNOS does not appear to modulate VCAM-1 expression in an immune model of chronic colitis.

Suppression of Proinflamatroy cytokine gene expression with Aqueous Extract of Berberin

2018 ◽  
Vol 9 (03) ◽  
pp. 20224-20238
Author(s):  
Samaneh Haj-allahyari ◽  
Dr Maghsoudi, Hossein
Keyword(s):  
Nitric Oxide ◽  
Experimental Period ◽  
Cytokine Gene Expression ◽  
Secretory Proteins ◽  
Dependent Manner ◽  
Berberis Vulgaris ◽  
Cyclooxygenase 1 ◽  
Tnf Α ◽  
Anti Inflammatory ◽  
Factor Α

Based on knowledge from traditional Iranian herbal medicine, this ex vitro study aims to examine the anti-inflammatory mechanism of Berberis vulgaris L by measuring the expression and release of pro-inflammatory cytokines, tumor necrosis factor-α (TNF-α), cyclooxygenase-1 (COX-1), and interleukine-18 (IL-6), IL-1β and inducible nitric oxide synthase (iNOS) in THP-1. The effects were assessed by measuring the levels of secretory proteins and mRNA of TNF-α and IL-6, the levels of nitric oxide (NO) secretion and the expression of iNOS in THP-1 cells. Cells were treated with 20 ng lipopolysaccharide/ml (LPS) in the presence and absence of concentrations of extracts from the Berberis vulgaris L. During the entire experimental period, we used extract concentrations (0.3 μg/mL) that had no cytotoxic effects, as measured with MTT, MTT and LDH assays. Berberis vulgaris extracts remarkably suppressed the LPS-induced NO release, significantly attenuated the LPS-induced transcription of iNOS and inhibited in a dose-dependent manner the expression and release of TNF-α. significant effects were observed on the release of IL-6. Taken together, these results suggest that Berberis vulgaris probably exerts anti-inflammatory effects through the suppression of TNF-α and iNOS expressions.

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