Piceatannol Prevents Lipopolysaccharide (LPS)‐Induced Nitric Oxide (NO) Production and Nuclear Factor (NF)‐κB Activation by Inhibiting IκB Kinase (IKK)

Islam, Shamima; Hassan, Ferdaus; Mu, Mya Mya; Ito, Hiroyasu; Koide, Naoki; Mori, Isamu; Yoshida, Tomoaki; Yokochi, Takashi

doi:10.1111/j.1348-0421.2004.tb03598.x

Cited by 50 publications

(24 citation statements)

References 37 publications

(53 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…24,25,30,31 In the murine macrophage cell line RAW264.7, LPS is shown to cause activation of ERK1/2, p38, and JNK/stress-activated protein kinase. 32 Moreover, LPS-induced TNF-␣ expression is suppressed in microglia by pretreatment with the p38 inhibitor SB203580, 33 and some studies have shown regulation of iNOS induction by MAPKs. 34,35 LPS has also been re- ported to elicit iNOS expression and to stimulate the release of NO via NF-B in RAW264.7 cells, 32 N9 microglial cells, 36 and human myometrial cells.…”

Section: Discussionmentioning

confidence: 99%

Mechanisms of endotoxin-induced NO, IL-6, and TNF-α production in activated rat hepatic stellate cells: Role of p38 MAPK

2006

View full text Add to dashboard Cite

Section: Discussionmentioning

confidence: 99%

Mechanisms of endotoxin-induced NO, IL-6, and TNF-α production in activated rat hepatic stellate cells: Role of p38 MAPK

2006

View full text Add to dashboard Cite

“…Inflammatory response stimulated by LPS is a suitable method to identify anti-inflammatory activity compounds in vitro. 11,[23][24][25] LPS stimulates macrophages and activates the expression of genes responsible for the synthesis of inflammatory mediators, such as reactive oxygen and nitrogen species. These free radicals are important mediators to provoke or sustain inflammatory processes, thereby protecting hosts from harmful stimuli.…”

Section: )mentioning

confidence: 99%

3β-Angeloyloxy-8β,10β-dihydroxyeremophila-7(11)-en-12,8α-lactone Inhibits Lipopolysaccharide-Induced Nitric Oxide Production in RAW264.7 Cells

Sun

Jiang

Zhao

et al. 2015

Biological & Pharmaceutical Bulletin

View full text Add to dashboard Cite

Farfugium japonicum (L.) KITAM, named "Lian-Peng-Cao" in China, has been traditionally used in Chinese folk medicine to treat sore throat, cold and cough due to its anti-inflammatory properties. In this study, the anti-inflammatory action of 3β-angeloyloxy-8β,10β-dihydroxyeremophila-7(11)-en-12,8α-lactone (FJ1) isolated from Farfugium japonicum and its molecular mechanism in RAW264.7 cells were investigated. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay showed that FJ1 with or without 3 µg/mL lipopolysaccharide (LPS) had no significant cytotoxicity in RAW264.7 cells. The production of nitric oxide (NO) was identified with a Griess reagent kit. The mRNA expression of inducible nitric oxide synthase (iNOS) and cytokines, including tumor necrosis factor α (TNF-α) and cyclooxygenase-2 (COX-2), was measured by real-time polymerase chain reaction (PCR). Reactive oxygen species (ROS) production was detected by flow cytometry analysis. Western blot was used to examine the protein expression of nuclear factor-kappa B (NF-κB)/p65, inhibitor of kappa B (IκB)-α, phosphorylated IκB-α (p-IκB-α), mitogen-activated protein kinase (MAPK) molecules, iNOS, and TNF-α. We discovered that FJ1 possesses anti-inflammatory effects that inhibit the release of LPS-stimulated pro-inflammatory cytokines, including NO and ROS. The molecular mechanism of FJ1-mediated anti-inflammation is associated with decreasing phosphorylation of MAPK molecules, including extracellular signal-related kinase 1/2 (ERK1/2), p38 MAPK, and c-Jun NH2-terminal kinase (JNK), FJ1 also reverses IκB degradation and attenuates the mRNA and protein expression of NF-κB-related downstream inducible enzymes and cytokines, such as iNOS, TNF-α in RAW264.7 cells. The results suggest that FJ1 has anti-inflammatory properties, which indicates that F. japonicum can be utilized to treat inflammatory diseases. The potential mechanism is associated with the NF-κB and MAPK activation pathways in LPS-stimulated macrophages.

show abstract

“…Syk is known to be expressed in vascular endothelial cells (16) and to participate in activation of the NF-κ B signal cascade upon thrombin stimulation (17), although its role in endothelial function is obscure. Also, Syk may participate in the regulation of inducible NOS (iNOS) expression: in bronchial epithelial cells, inhibition of Syk expression led to down-regulation of iNOS mRNA and NO production (18); and Syk inhibitors like piceatannol were found to prevent lipopolysaccharide (LPS)-induced NO generation in RAW 264.7 cells (19,20).…”

Section: Introductionmentioning

confidence: 99%

Shikonin Directly Inhibits Nitric Oxide Synthases: Possible Targets That Affect Thoracic Aorta Relaxation Response and Nitric Oxide Release From RAW 264.7 Macrophages

et al. 2010

View full text Add to dashboard Cite

Abstract.Recently, an isomeric mixture of herbal anti-inflammatory naphthoquinones shikonin and alkannin, and their derivatives, have been found to impair cellular responses involving nitric oxide (NO) and NO synthesis, like the acetylcholine-induced relaxation response of rat thoracic aorta and NO release from murine RAW 264.7 macrophages. However, the mechanisms of such effects, including whether NO synthase (NOS) activity is affected, remained unclear. We herein investigate possible targets of shikonin in these NOS-related events. Shikonin by itself dose-dependently inhibited the rat thoracic aorta relaxation in response to acetylcholine (pD′ 2 value: 6.29). Its optical enantiomer, alkannin, was equally inhibitory in the aorta relaxation-response assay. In RAW 264.7 cells, shikonin inhibited the lipopolysaccharide-induced NO production by 82% at 1 μ M. A cell-free assay to verify direct effects on NOS activity showed that shikonin inhibits all isoforms of NOS (IC 50 s, 4 -7 μ M), suggesting NOS as an inhibition target in both the events. Further possible targets of shikonin that might be involved in the inhibitions of the acetylcholineinduced aorta relaxation response and the NO generation by RAW 264.7 cells are also discussed. It is shown for the first time that shikonin inhibits NOS activity.

show abstract

Piceatannol Prevents Lipopolysaccharide (LPS)‐Induced Nitric Oxide (NO) Production and Nuclear Factor (NF)‐κB Activation by Inhibiting IκB Kinase (IKK)

Cited by 50 publications

References 37 publications

Mechanisms of endotoxin-induced NO, IL-6, and TNF-α production in activated rat hepatic stellate cells: Role of p38 MAPK

Mechanisms of endotoxin-induced NO, IL-6, and TNF-α production in activated rat hepatic stellate cells: Role of p38 MAPK

3β-Angeloyloxy-8β,10β-dihydroxyeremophila-7(11)-en-12,8α-lactone Inhibits Lipopolysaccharide-Induced Nitric Oxide Production in RAW264.7 Cells

Shikonin Directly Inhibits Nitric Oxide Synthases: Possible Targets That Affect Thoracic Aorta Relaxation Response and Nitric Oxide Release From RAW 264.7 Macrophages

Contact Info

Product

Resources

About