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Appears in Networks 6

In-Edges 17

p(HGNC:IFNG) increases act(p(HGNC:NOS2)) View Subject | View Object

In addition, T cell-derived IFNγ has been shown to downregulate the activity of NLRP3 via activation of inducible nitric oxide synthase (iNOS) in a mouse model of tuberculosis71; nitric oxide (NO) induces NLRP3 nitrosylation and thereby inhibits NLRP3 activity. PubMed:23702978

bp(GO:"astrocyte activation") increases sec(p(HGNC:NOS2)) View Subject | View Object

It is noteworthy that IL-1 beta and IL-18 can activate various cell types, par- ticularly astrocytes and microglia to induce additional cytokine release involving IL-1 beta , IL-6, and IL-18, and also nitric oxide (NO) synthase that can stimulate production of free radical NO, leading to the forma- tion of peroxynitrite that denatures DNA and impairs cellular energy pathways [48, 49]. PubMed:27314526

bp(GO:"microglial cell activation") increases sec(p(HGNC:NOS2)) View Subject | View Object

It is noteworthy that IL-1 beta and IL-18 can activate various cell types, par- ticularly astrocytes and microglia to induce additional cytokine release involving IL-1 beta , IL-6, and IL-18, and also nitric oxide (NO) synthase that can stimulate production of free radical NO, leading to the forma- tion of peroxynitrite that denatures DNA and impairs cellular energy pathways [48, 49]. PubMed:27314526

a(CHEBI:Anatabine) decreases p(HGNC:NOS2) View Subject | View Object

Anatabine suppressed in a dose- dependent manner the increase of iNOS and COX2 in- duced by interferon-g (Fig.4),confirming in vitro its antiinflammatory properties. The effect seen with inter- feron-g was also seen when macrophages were stimulated with lipopolysaccharide (Supplemental Fig. 1). PubMed:22807490

p(HGNC:IFNG) increases p(HGNC:NOS2) View Subject | View Object

Anatabine suppressed in a dose- dependent manner the increase of iNOS and COX2 in- duced by interferon-g (Fig.4),confirming in vitro its antiinflammatory properties. The effect seen with inter- feron-g was also seen when macrophages were stimulated with lipopolysaccharide (Supplemental Fig. 1). PubMed:22807490

a(CHEBI:"1,8-cineole") decreases p(HGNC:NOS2) View Subject | View Object

Further-more, the expression of NOS-2, COX2 and NF-B was reduced by1,8-cineole [250]. PubMed:29179999

a(CHEBI:"alpha-tocopherol") decreases p(HGNC:NOS2) View Subject | View Object

Furthermore, it disrupted the activity of NF-B, and thus, caused the suppression of NO synthase and inflammatory regulators such as IL-6 and IL-1, and the reduction of microglial activation [37] PubMed:29179999

a(CHEBI:curcumin) decreases p(HGNC:NOS2) View Subject | View Object

Curcumin showed several anti-inflammatory characteristics. It deploys various cytokine-inhibitory, anti-inflammatory activities and decreases the expression levels of COX-2, LOX, and iNOS. Moreover, the expression of the pro-inflammatory cytokines, for instance, TNF-, IL-1, -2,-6, -8, and -12 and the neurotoxic factors were suppressed by curcumin in lipopolysaccharide (LPS)-stimulated monocytes and alveolar macrophages [103]. PubMed:29179999

a(CHEBI:resveratrol) decreases p(HGNC:NOS2) View Subject | View Object

It also lowered the expression of NO and iNOS, and prostaglandin E2 (PGE2) and COX2 in A-activated glial cells. All these effects were attributableto their suppression of nuclear NF-B translocation [116]. PubMed:29179999

a(PUBCHEM:102336202) decreases p(HGNC:NOS2) View Subject | View Object

It down-regulated iNOS expression and nitrotyrosin levels in the hip-pocampus and stimulated the mRNA expression level of IL-4 [247]. PubMed:29179999

a(PUBCHEM:14193399) decreases p(HGNC:NOS2) View Subject | View Object

Glaucocalyxin B, found in Rabdosia japonica, considerably atten-uated the expression of NO, TNF-, IL-1, COX-2 and iNOS in LPS-induced microglia cells [169–172]. Moreover, the activation of NF-B, p38 MAPK and ROS generation was interrupted by glauco- calyxin B in LPS-induced microglia cells [172]. PubMed:29179999

a(PUBCHEM:164676) decreases act(p(HGNC:NOS2)) View Subject | View Object

It inhibited the activation of iNOS, matrix metalloproteinase 2 (MMP2), and NF-Bp65 and consequently prevent AD in the brain [229–231]. PubMed:29179999

a(PUBCHEM:440312) decreases p(HGNC:NOS2) View Subject | View Object

LPS-activated expression of pro-inflammatory and neurotoxic factors like NO, TNF-, PGE2, NO synthase and COX2 production and LOX activity were inhibited by dihydroasparagusic acid in microglia cells [243]. PubMed:29179999

a(CHEBI:"(+)-Tetrandrine") decreases p(HGNC:NOS2) View Subject | View Object

Tetrandrine, is an herb-derived bisbenzylioquinoline alkaloid, may be a potent inhibitor of NF-κB activation and can inhibit the expression of iNOS and COX-2 which are involved in pro-inflammation. PubMed:27288790

p(FPLX:NFkappaB) regulates act(p(HGNC:NOS2)) View Subject | View Object

ROS has been found not only the regulators of NF-κB, interestingly, iNOS is also regulated by NF-κB. PubMed:27288790

act(complex(GO:"NF-kappaB complex")) increases act(p(HGNC:NOS2)) View Subject | View Object

Excessive accumulation of Aβ1-42 stimulates microglial cells by signaling via receptor associated advanced glycation end products (RAGE) and peroxisome proliferator-activated receptor-γ (PPAR-γ), phosphorylates IKK proteins, and enhances NF-κB mediated transactivation of inflammatory cytokines and neurotoxic molecules such as glutamate and reactive oxygen species (ROS)/induced nitric oxide synthase (iNOS) [12] (Fig 2B) PubMed:25652642

act(complex(GO:"NF-kappaB complex")) increases act(p(HGNC:NOS2)) View Subject | View Object

Furthermore NF-κB specific inhibitor prevents iNOS and ROS upregulation in Aβ stimulated cultures of astrocytes or mixed cortical cells PubMed:25652642

Out-Edges 3

act(p(HGNC:NOS2)) increases a(CHEBI:"nitric oxide") View Subject | View Object

In addition, T cell-derived IFNγ has been shown to downregulate the activity of NLRP3 via activation of inducible nitric oxide synthase (iNOS) in a mouse model of tuberculosis71; nitric oxide (NO) induces NLRP3 nitrosylation and thereby inhibits NLRP3 activity. PubMed:23702978

act(p(HGNC:NOS2)) increases a(CHEBI:"nitric oxide") View Subject | View Object

It is noteworthy that IL-1 beta and IL-18 can activate various cell types, par- ticularly astrocytes and microglia to induce additional cytokine release involving IL-1 beta , IL-6, and IL-18, and also nitric oxide (NO) synthase that can stimulate production of free radical NO, leading to the forma- tion of peroxynitrite that denatures DNA and impairs cellular energy pathways [48, 49]. PubMed:27314526

p(HGNC:NOS2) increases path(MESH:Inflammation) View Subject | View Object

Tetrandrine, is an herb-derived bisbenzylioquinoline alkaloid, may be a potent inhibitor of NF-κB activation and can inhibit the expression of iNOS and COX-2 which are involved in pro-inflammation. PubMed:27288790

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If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.