Increased expression of interleukin-1β in triglyceride-induced macrophage cell death is mediated by p38 MAP kinase

Sung, Ho Joong; Son, Sin Jee; Yang, Seung Ju; Rhee, Ki Jong; Kim, Yoon Suk

doi:10.5483/bmbrep.2012.45.7.088

Cited by 4 publications

(4 citation statements)

References 32 publications

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“…As a pro-inflammatory cytokine, it is engaged in the formation of PGs and degrading enzymes such as collagenase. Thus, it is known to activate T-cells and B-cells and to induce inflammatory responses [30,31]. Our results confirmed that ferulic acid inhibits IL-1β production ( Fig 5B).…”

Section: Inhibitory Effect Of Ferulic Acid On Inos and Cox-2 Protein supporting

confidence: 85%

The inflammatory activity of purified-ferulic acid from Tetragonia tetragonioides

Kim

Park

Lee

et al. 2019

JABC

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In this study, an evaluation of the anti-inflammatory effect of ferulic acid isolated from Tetragonia tetragonioides in lipopolysaccharide (LPS) simulated RAW 264.7 cells was made. The chemical structure of the active compound was elucidated by 1 H-NMR, 13 C-NMR, and FAB-MS, and was confirmed to be ferulic acid. Ferulic acid was purified via open column chromatography with Sephadex LH-20 and MCI gel CHP-20. To test the antiinflammatory effect of ferulic acid, LPS-stimulated RAW 264.7 cells were treated in subsequent experiments with different concentrations of ferulic acid (5, 10, and 25 μg/mL) and the levels of inflammatory cytokines and enzymes were also measured by the 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide assay. Cell viability was above 95% at acid concentrations ranging from 5-25 μg/mL. The results showed that 30% of the production of nitric oxide and 66% of prostaglandin E 2 were inhibited by 25 μg/mL of ferulic acid, it also inhibited the protein expression of both inducible nitric oxide synthase and cyclooxygenase-2 by 70%. Additionally, it inhibited the production of the pro-inflammatory cytokines, tumor necrosis factor-α, interleukin-6, and interleukin-1β by 40, 75, and 77%, respectively. According to these results, the anti-inflammatory activity of ferulic acid was demonstrated via his implication in the inhibition of the expression and secretion of inflammatory substances in LPS-stimulated RAW 264.7 cells. Therefore, we concluded that ferulic acid can be used as a functional additive having anti-inflammatory activity.

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Section: Inhibitory Effect Of Ferulic Acid On Inos and Cox-2 Protein supporting

confidence: 85%

The inflammatory activity of purified-ferulic acid from Tetragonia tetragonioides

Kim

Park

Lee

et al. 2019

JABC

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“…The expression of IL-1β decreased markedly in response to TG treatment, as previously reported. 21) However, the expression of the IL-1R1, TNF-α, IL-18, and MIP-1α remained unchanged ( Fig. 2A).…”

Section: Tg Induces Decreased Expression Of Il-1β Mrna Butmentioning

confidence: 99%

“…11) We previously showed that THP-1 macrophages treated with TG (1 mg/mL) for 24 h exhibited reduced viability. 21) To expand upon this observation, differentiated THP-1 cells were treated with TG in a dose-and timedependent manner. Viable cells were enumerated using trypan blue dye.…”

Section: Accumulation Of Tg Induces Macrophage Cell Deathmentioning

confidence: 99%

“…21) We determined if p38 MAPK is involved in TGinduced cell death using a p38 MAPK inhibitor (SB203580). Our results indicate that the addition of the p38 MAPK inhibitor does not prevent TG-mediated cell death suggesting that the p38 MAPK which is involved in down-regulation of IL-1β mRNA expression is not involved in cell viability (Fig.…”

Section: Tg Induces Decreased Expression Of Il-1β Mrna Butmentioning

confidence: 99%

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Triglyceride-Induced Macrophage Cell Death Is Triggered by Caspase-1

Son

Rhee

Lim

et al. 2013

Biological & Pharmaceutical Bulletin

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Triglyceride (TG) induces macrophage cell death which contributes to the development of atherosclerosis. We confirmed that exogenous TG accumulates in human THP-1 macrophages and causes cell death. TG treated THP-1 macrophages exhibited no change in tumor necrosis factor (TNF)-α, interleukin (IL)-18, macrophage inflammatory protein (MIP)-1α, and IL-1R1 receptor mRNA expression. However, there was a marked decrease in IL-1β mRNA expression but an increase in IL-1β protein secretion. Decreased expression of IL-1β mRNA and increased secretion of IL-1β protein was not the direct cause of cell death. Until now, TG was assumed to induce necrotic cell death in macrophages. Since caspase-1 is known to be involved in activation and secretion of IL-1β protein and pyroptotic cell death, next we determined whether caspase-1 is associated with TG-induced macrophage cell death. We found an increase in caspase-1 activity in TGtreated THP-1 macrophages and inhibition of caspase-1 activity using a specific inhibitor partially rescued cell death. These results suggest activation of the pyroptotic pathway by TG. This is the first report implicating the activation of caspase-1 and the triggering of the pyroptosis pathway in TG-induced macrophage cell death.

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Role of oxidative stress in infectious diseases. A review

Pohanka

2013

Folia Microbiol

126

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Oxidative stress plays a dual role in infections. Free radicals protect against invading microorganisms, and they can also cause tissue damage during the resulting inflammation. In the process of infection, there is generation of reactive species by myeloperoxidase, NADPH oxidase, and nitric oxide synthase. On the other hand, reactive species can be generated among others, by cytochrome P450, some metals, and xanthine oxidase. Some pathologies arising during infection can be attributed to oxidative stress and generation of reactive species in infection can even have fatal consequences. This article reviews the basic pathways in which reactive species can accumulate during infectious diseases and discusses the related health consequences.

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Increased expression of interleukin-1β in triglyceride-induced macrophage cell death is mediated by p38 MAP kinase

Cited by 4 publications

References 32 publications

The inflammatory activity of purified-ferulic acid from Tetragonia tetragonioides

The inflammatory activity of purified-ferulic acid from Tetragonia tetragonioides

Triglyceride-Induced Macrophage Cell Death Is Triggered by Caspase-1

Role of oxidative stress in infectious diseases. A review

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