4-Hydroxykobusin Inhibits the Induction of Nitric Oxide Synthase by Inhibiting NF-.KAPPA.B and AP-1 Activation

Pokharel, Yuba Raj; Liu, Qing-He; Oh, Jae Wook; Woo, Eun‐Rhan; Kang, Keon Wook

doi:10.1248/bpb.30.1097

Cited by 21 publications

(18 citation statements)

References 41 publications

(21 reference statements)

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“…Our data also confirmed that increased AP-1/JunD level was accompanied by elevated proliferative capacity in DETA/NO -treated melanoma cells. Additionally, some attempts to correlate NO with AP-1 in other cellular system uncovered a positive relationship between them: NO increased AP-1 activity (28,29) and the inhibition of AP-1 led to the inhibition of NO formation as well (30). In melanoma cells, AP-1/JunD was activated and its DNA-binding activity was enhanced with the trend nearly paralleling that of APE/Ref Bcl-2, an important downstream molecule regulated by NF-nB, is closely tied to apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Nitric oxide initiates progression of human melanoma via a feedback loop mediated by apurinic/apyrimidinic endonuclease-1/redox factor-1, which is inhibited by resveratrol

Yang

Misner³

et al. 2008

Molecular Cancer Therapeutics

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Section: Discussionmentioning

confidence: 99%

Nitric oxide initiates progression of human melanoma via a feedback loop mediated by apurinic/apyrimidinic endonuclease-1/redox factor-1, which is inhibited by resveratrol

Yang

Misner³

et al. 2008

Molecular Cancer Therapeutics

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“…Employing the intrastriatal injection of autologous blood in rats to model intracerebral hemorrhage, Zhao et al [69] demonstrated a robust and prolonged NF-κB activation and a robust induction of iNOS at both the mRNA and protein levels. In SCI models, iNOS was also found to be increased [70] , and the drugs inhibiting NOS offered protective effects [71][72][73] .…”

Section: Nf-κb Biologymentioning

confidence: 98%

Dual roles of NF-κB in cell survival and implications of NF-κB inhibitors in neuroprotective therapy

Qin

Tao

Chen

2007

Acta Pharmacologica Sinica

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NF-κB is a well-characterized transcription factor with multiple physiological and pathological functions. NF-κB plays important roles in the development and maturation of lymphoids, regulation of immune and inflammatory response, and cell death and survival. The influence of NF-κB on cell survival could be protective or destructive, depending on types, developmental stages of cells, and pathological conditions. The complexity of NF-κB in cell death and survival derives from its multiple roles in regulating the expression of a broad array of genes involved in promoting cell death and survival. The activation of NF-κB has been found in many neurological disorders, but its actual roles in pathogenesis are still being debated. Many compounds with neuroprotective actions are strongly associated with the inhibition of NF-κB, leading to speculation that blocking the pathological activation of NF-κB could offer neuroprotective effects in certain neurodegenerative conditions. This paper reviews the recent developments in understanding the dual roles of NF-κB in cell death and survival and explores its possible usefulness in treating neurological diseases. This paper will summarize the genes regulated by NF-κB that are involved in cell death and survival to elucidate why NF-κB promotes cell survival in some conditions while facilitating cell death in other conditions. This paper will also focus on the effects of various NF-κB inhibitors on neuroprotection in certain pathological conditions to speculate if NF-κB is a potential target for neuroprotective therapy.

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“…The plant has traditionally been used as an anti-diarrhetic agent in East Asia (9). Moreover, it has been reported to exhibit anti-mutagenic, anti-inflammatory, and anti-oxidative effects (10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

Anti-obesity effects of Geranium thunbergii extract via improvement of lipid metabolism in high-fat diet-induced obese mice

Kim¹

2011

Mol Med Report

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Abstract. This study investigated the anti-obesity properties of an extract of Geranium thunbergii (GTE) in high-fat diet-induced obese mice. GTE treatment significantly reduced body weight, adipose tissue mass, adipocyte size, as well as serum triglyceride, total cholesterol and low-density lipoprotein-cholesterol levels in obese mice compared to high-fat diet-fed mice. It also decreased serum leptin levels and increased adiponectin levels. The serum levels of aspartate transaminase, alanine transaminase, blood urea nitrogen and creatinine were not significantly changed in GTE-treated mice compared to serum levels in normal diet and high-fat diet-fed mice. Furthermore, GTE suppressed the mRNA levels of sterol regulatory element-binding protein 1c, peroxisome proliferator-activated receptor γ, adipocyte fatty acid-binding protein and fatty acid synthase in the adipose tissues of obese mice. These results suggest that GTE ameliorated high-fat diet-induced obesity by altering the adipokine levels and downregulating the expression of transcription factors and lipogenic enzymes involved in lipid metabolism.

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4-Hydroxykobusin Inhibits the Induction of Nitric Oxide Synthase by Inhibiting NF-.KAPPA.B and AP-1 Activation

Cited by 21 publications

References 41 publications

Nitric oxide initiates progression of human melanoma via a feedback loop mediated by apurinic/apyrimidinic endonuclease-1/redox factor-1, which is inhibited by resveratrol

Nitric oxide initiates progression of human melanoma via a feedback loop mediated by apurinic/apyrimidinic endonuclease-1/redox factor-1, which is inhibited by resveratrol

Dual roles of NF-κB in cell survival and implications of NF-κB inhibitors in neuroprotective therapy

Anti-obesity effects of Geranium thunbergii extract via improvement of lipid metabolism in high-fat diet-induced obese mice

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