Regulation of Macrophage Eicosanoid Generation Is Dependent on Nuclear Factor kappa B

Lo, Chang-fa; Cryer, H. Gill; Fu, Minjuan; Lo, Fei-Yun

doi:10.1097/00005373-199807000-00004

Cited by 53 publications

(37 citation statements)

References 19 publications

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“…(3) In general, NSAID doses at the IC 50 , including ibuprofen, are known to reduce COX activity by blocking COX enzyme. However, ibuprofen can also reduce COX-2 mRNA levels (Kannan et al, 2004;Lo et al, 1998). COX-2 mRNA levels were measured in our ibuprofen treated mice, however, they were not significantly reduced (À13%, n ¼ 8, p ¼ 0.38; see supplemental data).…”

Section: Discussionmentioning

confidence: 70%

Ibuprofen Suppresses Interleukin-1β Induction of Pro-Amyloidogenic α1-Antichymotrypsin to Ameliorate β-Amyloid (Aβ) Pathology in Alzheimer's Models

Morita

Teter

Yang

et al. 2005

Neuropsychopharmacol

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Epidemiological and basic research suggests that nonsteroidal anti-inflammatory drugs (NSAIDs) should protect against the most common forms of Alzheimer's disease (AD). Ibuprofen reduces amyloid (Ab) pathology in some transgenic models, but the precise mechanisms remain unclear. Although some reports show select NSAIDs inhibit amyloid production in vitro, the possibility that in vivo suppression of amyloid pathology occurs independent of Ab production has not been ruled out. We show that ibuprofen reduced Ab brain levels in rats from exogenously infused Ab in the absence of altered Ab production. To determine whether ibuprofen inhibits proamyloidogenic factors, APPsw (Tg2576) mice were treated with ibuprofen for 6 months, and expression levels of the Ab and inflammation-related molecules a 1 antichymotrypsin (ACT), apoE, BACE1, and peroxisome proliferator-activated receptor g) (PPARg) were measured. Among these, ACT, a factor whose overexpression accelerates amyloid pathology, was reduced by ibuprofen both in vivo and in vitro. IL-1b, which was reduced in our animals by ibuprofen, induced mouse ACT in vitro. While some NSAIDs may inhibit Ab42 production, these observations suggest that ibuprofen reduction of Ab pathology may not be mediated by altered Ab42 production. We present evidence supporting the hypothesis that ibuprofen-dependent amyloid reduction is mediated by inhibition of an alternate pathway (IL-1b and its downstream target ACT).

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Section: Discussionmentioning

confidence: 70%

Ibuprofen Suppresses Interleukin-1β Induction of Pro-Amyloidogenic α1-Antichymotrypsin to Ameliorate β-Amyloid (Aβ) Pathology in Alzheimer's Models

Morita

Teter

Yang

et al. 2005

Neuropsychopharmacol

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“…NS-398 is well known to inhibit COX-2 activity and expression, selectively. It has been reported that NS-398 blocks COX-2 mRNA expression and enzyme activity as well as PGE 2 production in RAW264.7 macrophages (25,26).…”

Section: Discussionmentioning

confidence: 98%

“…3: B and D). NS-398, a COX-2 selective inhibitor (25,26), significantly inhibited the expression of COX-2 (Figs. 2B and 3B) and production of PGE 2 (Figs.…”

Section: Effects Of Asperlin On Expression Of Proinflammatory Enzymesmentioning

confidence: 95%

“…Primary antibodies including HO-1, COX-2, iNOS, IκB-α, p-IκB-α, p65, β-actin, proliferating cell nuclear antigen (PCNA), lamin B, and secondary antibodies used for western blot analysis were purchased from Santa Cruz Biotechnology (Santa Cruz, CA, USA). NS-398 (N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide), a COX-2-selective inhibitor (25,26), was purchased from Calbiochem (Darmstadt, Germany). Enzyme-linked immunosorbent assay (ELISA) kits for PGE 2 , TNF-α, and IL1-β were purchased from R&D Systems (Minneapolis, MN, USA).…”

Section: Chemicals and Reagentsmentioning

confidence: 99%

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Asperlin From the Marine-Derived Fungus Aspergillus sp. SF-5044 Exerts Anti-inflammatory Effects Through Heme Oxygenase-1 Expression in Murine Macrophages

Lee¹,

Jeong²,

Li³

et al. 2011

J Pharmacol Sci

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“…COX-2-induced PG production has been implicated in inflammation, as elevated levels of this protein have been found in synovial cells treated with inflammatory mediators or from patients with rheumatoid arthritis (33)(34)(35)(36)(37). The expression of the cox-2 gene appears to be highly regulated by a number of transcription factors, in particular by NF-B (35,(37)(38)(39)(40).…”

mentioning

confidence: 99%

Prostaglandin Levels in Stimulated Macrophages Are Controlled by Phospholipase A2-activating Protein and by Activation of Phospholipase C and D

Ribardo

Crowe

Kuhl

et al. 2001

Journal of Biological Chemistry

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Regulation of Macrophage Eicosanoid Generation Is Dependent on Nuclear Factor kappa B

Abstract: Our data indicate that COX-2 gene expression by LPS-stimulated Mphi is dependent on NFkappaB. Cyclooxygenase inhibitors reduced PGE2 production by inhibiting both COX-2 mRNA expression and preventing NFkappaB activation.

Cited by 53 publications

References 19 publications

Ibuprofen Suppresses Interleukin-1β Induction of Pro-Amyloidogenic α1-Antichymotrypsin to Ameliorate β-Amyloid (Aβ) Pathology in Alzheimer's Models

Ibuprofen Suppresses Interleukin-1β Induction of Pro-Amyloidogenic α1-Antichymotrypsin to Ameliorate β-Amyloid (Aβ) Pathology in Alzheimer's Models

Asperlin From the Marine-Derived Fungus Aspergillus sp. SF-5044 Exerts Anti-inflammatory Effects Through Heme Oxygenase-1 Expression in Murine Macrophages

Prostaglandin Levels in Stimulated Macrophages Are Controlled by Phospholipase A2-activating Protein and by Activation of Phospholipase C and D

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