Diphlorethohydroxycarmalol Inhibits Interleukin-6 Production by Regulating NF-κB, STAT5 and SOCS1 in Lipopolysaccharide-Stimulated RAW264.7 Cells

Kang, Na Ri; Han, Sang‐Kyoo; Kang, Gyeoung Jin; Koo, Dong Hwan; Koh, Young Sang; Hyun, Jin Won; Lee, Nam Ho; Ko, Mi Hee; Kang, Hee Kyoung; Yoo, Eun Sook

doi:10.3390/md13042141

Cited by 41 publications

(28 citation statements)

References 34 publications

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“…Several previous reports have shown that NF-κB and STAT1 act as important upstream signaling molecules for the production of IL-6 in LPS-stimulated monocytes or macrophages. In a previous study, we reported that N-tosyl-L-phenylalanine chloromethyl ketone, a specific inhibitor of NF-κB signaling, affects IL-6 production ( 23 ). NF-κB inhibition attenuates TLR4 expression in LPS-treated THP1 monocytes ( 22 ).…”

Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Effect of 3-Bromo-4,5-Dihydroxybenzaldehyde, a Component ofPolysiphonia morrowii,In VivoandIn Vitro

et al. 2017

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3-Bromo-4,5-dihydroxybenzaldehyde (BDB) is a natural bromophenol compound that is most commonly isolated from red algae. The present study was designed to investigate the anti-inflammatory properties of BDB on atopic dermatitis (AD) in mice induced by 2,4-dinitrochlorobenzene (DNCB) and on lipopolysaccharide (LPS)-stimulated murine macrophages. BDB treatment (100 mg/kg) resulted in suppression of the development of AD symptoms compared with the control treatment (induction-only), as demonstrated by reduced immunoglobulin E levels in serum, smaller lymph nodes with reduced thickness and length, a decrease in ear edema, and reduced levels of inflammatory cell infiltration in the ears. In RAW 264.7 murine macrophages, BDB (12.5, 25, 50, and 100 μM) suppressed the production of interleukin-6, a proinflammatory cytokine, in a dose-dependent manner. BDB also had an inhibitory effect on the phosphorylation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and signal transducer and activator of transcription 1 (STAT1; Tyr 701), two major signaling molecules involved in cellular inflammation. Taken together, the results show that BDB treatment alleviates inflammatory responses in an atopic dermatitis mouse model and RAW 264.7 macrophages. These results suggest that BDB may be a useful therapeutic strategy for treating conditions involving allergic inflammation such as atopic dermatitis.

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Section: Discussionmentioning

confidence: 99%

Anti-Inflammatory Effect of 3-Bromo-4,5-Dihydroxybenzaldehyde, a Component ofPolysiphonia morrowii,In VivoandIn Vitro

et al. 2017

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“…5, changes in the TNF-α and IL-6 levels were not detected as the PDR extract concentration (3, 5, 7, and 10 μg/mL) was increased. Kang et al [32] reported that 100 μM of diphlorethohydroxycarmalol had no effect on TNF-α production, which was similar to the PDR extract. Likewise, Wong et al [33] reported no significant difference in the levels of IL-6 by vomitoxin treatment in RAW 264.7 cells, similar to the PDR extract effect.…”

Section: Resultsmentioning

confidence: 89%

Inhibition of inflammatory responses in lipopolysaccharide-induced RAW 264.7 cells byPinus densifloraroot extract

Lee

Park

et al. 2018

JABC

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Pinus densiflora root (PDR) is used as a medicinal plant. In this study, we investigated whether the PDR extract has anti-inflammatory activities. Cell viability assays showed that the extract was not toxic toward RAW 264.7 cells at concentrations up to 10 μg/mL. At 10 μg/mL, the extract decreased nitric oxide (NO) content to 40% of the control level. The protein expression of inducible nitric oxide synthase (iNOS), which generates NO, decreased with increasing concentrations of the extract. Prostaglandin E 2 (PGE 2 ) levels were significantly inhibited by over 50% in the presence of 10 μg/mL of the extract. The protein expression of cyclooxygenase-2 (COX-2), which generates PGE 2 , decreased with increasing concentrations of the extract. Proinflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and IL-1β, were detected in RAW 264.7 cells after lipopolysaccharide (LPS) treatment. The extract did not affect the levels of TNF-α and IL-6, but it significantly inhibited the level of IL-1β. It also completely inhibited the transcription of nuclear factor-kappaB (NF-κB). These results indicate that the PDR extract reduces inflammatory response-related proteins, such as NO, PGE 2 , iNOS, and COX-2, in LPS-induced RAW 264.7 cells via the regulation of NF-κB. Consequently, we have provided a mechanism to explain the anti-inflammatory effect of the PDR extract; that is, it exerts such an effect by regulating NF-κB. The PDR extract can therefore be considered as an effective antiinflammatory agent.

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“…SOCS1 inhibits excessive cytokine signaling, based on the fact that SOCS1-knockout (KO) mice die of severe inflammation within three weeks of birth [ 1 ]. SOCS1 decreases IL-6 production in LPS-stimulated RAW 264.7 cells [ 2 ]. Secretory SOCS1 exerts anti-inflammatory effects [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

miR-122-SOCS1-JAK2 axis regulates allergic inflammation and allergic inflammation-promoted cellular interactions

Noh

Kim

et al. 2017

Oncotarget

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The regulatory role of suppressor of cytokine signaling 1 (SOCS1) in inflammation has been reported. However, its role in allergic inflammation has not been previously reported. SOCS1 mediated in vitro and in vivo allergic inflammation. Histone deacetylase-3 (HDAC3), a mediator of allergic inflammation, interacted with SOCS1, and miR-384 inhibitor, a positive regulator of HDAC3, induced features of allergic inflammation in an SOCS1-dependent manner. miRNA array analysis showed that the expression of miR-122 was decreased by antigen-stimulation. TargetScan analysis predicted the binding of miR-122 to the 3′-UTR of SOCS1. miR-122 inhibitor induced in vitro and in vivo allergic features in SOCS1-dependent manner. SOCS1 was necessary for allergic inflammation-promoted enhanced tumorigenic and metastatic potential of cancer cells. SOCS1 and miR-122 regulated cellular interactions involving cancer cells, mast cells and macrophages during allergic inflammation. SOCS1 mimetic peptide, D-T-H-F-R-T-F-R-S-H-S-D-Y-R-R-I, inhibited in vitro and in vivo allergic inflammation, allergic inflammation-promoted enhanced tumorigenic and metastatic potential of cancer cells, and cellular interactions during allergic inflammation. Janus kinase 2 (JAK2) exhibited binding to SOCS1 mimetic peptide and mediated allergic inflammation. Transforming growth factor- Δ1 (TGF-Δ1) was decreased during allergic inflammation and showed an anti-allergic effect. SOCS1 and JAK2 regulated the production of anti-allergic TGF-Δ1. Taken together, our results show that miR-122-SOCS1 feedback loop can be employed as a target for the development of anti-allergic and anti-cancer drugs.

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Diphlorethohydroxycarmalol Inhibits Interleukin-6 Production by Regulating NF-κB, STAT5 and SOCS1 in Lipopolysaccharide-Stimulated RAW264.7 Cells

Cited by 41 publications

References 34 publications

Anti-Inflammatory Effect of 3-Bromo-4,5-Dihydroxybenzaldehyde, a Component ofPolysiphonia morrowii,In VivoandIn Vitro

Anti-Inflammatory Effect of 3-Bromo-4,5-Dihydroxybenzaldehyde, a Component ofPolysiphonia morrowii,In VivoandIn Vitro

Inhibition of inflammatory responses in lipopolysaccharide-induced RAW 264.7 cells byPinus densifloraroot extract

miR-122-SOCS1-JAK2 axis regulates allergic inflammation and allergic inflammation-promoted cellular interactions

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