5-Bromo-2-hydroxy-4-methyl-benzaldehyde inhibited LPS-induced production of pro-inflammatory mediators through the inactivation of ERK, p38, and NF-κB pathways in RAW 264.7 macrophages

Kim, Kil-Nam; Ko, Seok‐Chun; Ye, Bo-Ram; Kim, Min-Sun; Kim, Junseong; Ko, Eun-Yi; Cho, Su-Hyeon; Kim, Daekyung; Heo, Soo‐Jin; Jung, Won‐Kyo

doi:10.1016/j.cbi.2016.08.022

Cited by 30 publications

(24 citation statements)

References 31 publications

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“…The pro-inflammatory cytokines including TNF-α, IL-1β, and IL-6 mediate and regulate immunity and inflammation during the inflammatory process (Trikha et al 2003;Huang et al 2006). These cytokines play key roles in the induction of inflammatory process (Kim et al 2016). Among the several inflammatory cytokines, TNF-α is known to synthesize in the macrophages, and it stimulates the production of other inflammatory cytokines, such as IL-1β and IL-6 (Aggarwal and Natarajan 1996).…”

Section: Resultsmentioning

confidence: 99%

“…Western blot analysis was conducted to protein expression as described by Kim et al (2016). RAW 264.7 macrophages were seeded in a 96-well plate and incubated with LPS (1 μg/mL) coupled with aliquots of the ozonated krill oil at 37°C for 24 h. Then, the cells were collected and washed twice with PBS.…”

Section: Western Blot Analysismentioning

confidence: 99%

“…RT-PCR analysis was conducted to determine the mRNA expression as described by Kim et al (2016). The total ribonucleic acid (RNA) from the RAW 264.7 macrophages treated with LPS in the presence or absence of ozonated krill oil was extracted using the TRIzol reagent.…”

Section: Reverse Transcription-polymerase Chain Reaction (Rt-pcr) Anamentioning

confidence: 99%

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Anti-inflammatory effect of ozonated krill (Euphausia superba) oil in lipopolysaccharide-stimulated RAW 264.7 macrophages

Kim

Lee

et al. 2018

Fish Aquatic Sci

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Background: Inflammation has been known to associate with many human diseases. The objective of this study was to evaluate an anti-inflammatory effect of ozonated krill (Euphausia superba) oil, which was prepared by the treatment of krill oil using ozone gas. The anti-inflammatory activity was evaluated in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. Results: Ozonated krill oil significantly inhibited nitric oxide (NO) production and suppressed the mRNA and protein expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) in LPS-stimulated RAW 264.7 macrophages. Ozonated krill oil also reduced the mRNA expression of inflammatory cytokines such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α in LPS-stimulated RAW 264.7 macrophages. To elucidate the mechanism underlying the anti-inflammatory activity of ozonated krill oil, we evaluated the effects of ozonated krill oil on the activation of mitogen-activated protein kinases (MAPKs) pathway. Ozonated krill oil suppressed the LPS-stimulated phosphorylation of p38 MAPK and c-Jun N-terminal kinases (JNK).

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Section: Resultsmentioning

confidence: 99%

Section: Western Blot Analysismentioning

confidence: 99%

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Anti-inflammatory effect of ozonated krill (Euphausia superba) oil in lipopolysaccharide-stimulated RAW 264.7 macrophages

Kim

Lee

et al. 2018

Fish Aquatic Sci

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“…It has been demonstrated that ERK plays a crucial role in transferring inflammatory information from the extracellular environment to the cytoplasm or nucleus, which can modulate inflammatory responses (35,36). The ERK signaling pathway can regulate PASMCs exposed to 5-HT during mitosis (37).…”

Section: Discussionmentioning

confidence: 99%

The protective effects of PCPA against monocrotaline-induced pulmonary arterial hypertension are mediated through the downregulation of NFAT-1 and NF-κB

Bai

Wang

et al. 2017

International Journal of Molecular Medicine

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Inflammation and remodeling play a role in the pathogenesis of pulmonary arterial hypertension (PAH). Nuclear factor-κB (NF-κB) and nuclear factor of activated T cells-1 (NFAT-1) participate in inflammation and remodeling in a number of diseases. As a tryptophan hydroxylase inhibitor, 4-chloro-DL-phenylalanine (PCPA) had been reported to exert anti-inflammatory and remodeling effects. Therefore, we hypothesized that PCPA may attenuate monocrotaline (MCT)-induced PAH through the NFAT-1 and NF-κB signaling pathways. In order to confirm our hypothesis, we divided 68 Sprague-Dawley male rats into 4 groups as follows: the control, MCT, MCT + P1 and MCT + P2 groups. MCT was administered at a dose of 60 mg/kg once via intraperitoneal injection. PCPA was administered via intraperitoneal injection at a dose of 50 or 100 mg/kg once daily for 21 consecutive days. We then measured the hemodynamic index and morphological analysis was carried out on the lung tissues. Western blot analysis and immunohistochemistry were used to examine the levels of NFAT-1 and NF-κB p-65. The expression levels of phosphorylated inhibitor of NF-κB kinase (p-IKK), IKK, phosphorylated extracellular signal-regulated kinase (p-ERK), ERK, intercellular adhesion molecule-1 (ICAM-1) and interleukin-6 (IL-6) were examined by western blot analysis. MCT was found to significantly induce PAH, with inflammation and remodeling of the lung tissues. This was associatd with an increased expression of NFAT-1, p-IKK, p-ERK and nuclear p65. PCPA significantly attenuated MCT-induced inflammation and arterial remodeling, and decreased the expression of NFAT-1, as well as that of relevant proteins of the NF-κB signaling pathway. The above-mentioned findings suggest that the inhibitory effects of PCPA on MCT-induced inflammation and arterial remodeling are related to the downregulation of the NFAT-1 and NF-κB signaling pathways in rats with PAH.

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“…It is well known that the NF-κB pathway serves an important role in regulating immune and inflammatory processes, and affects the expression of cytokines that mediate pro-inflammatory responses and inflammation, apoptosis and proliferation (30). The NF-κB (p65) signalling pathway is highly activated in the inflammatory sites with diverse enzymes, which induces the transcription and production of inflammatory cytokines, including IL-1β, IL-6 and TNF-α at the inflammatory site; this pathway is known to serve an important role during the acute phase of the immune response (31).…”

Section: Discussionmentioning

confidence: 99%

Angiotensin II induces RAW264.7 macrophage polarization to the M1‑type through the connexin 43/NF‑κB pathway

Chen

Xiao

et al. 2020

Mol Med Report

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angiotensin ii (angii) serves an important inflammatory role in cardiovascular disease; it can induce macrophages to differentiate into the M1-type, produce inflammatory cytokines and resist pathogen invasion, and can cause a certain degree of damage to the body. Previous studies have reported that connexin 43 (Cx43) and NF-κB (p65) are involved in the AngII-induced inflammatory pathways of macrophages; however, the mechanisms underlying the effects of Cx43 and NF-κB (p65) on AngII-induced macrophage polarization have not been determined. Thus, the present study aimed to investigate the effects of Cx43 and NF-κB (p65) on the polarization process of AngII-induced macrophages. The macrophage polarization-related proteins and mRNAs were examined by flow cytometry, western blotting, immunofluorescence, ELISA and reverse transcription-quantitative PCR analyses. RAW264.7 macrophages were treated with AngII to simulate chronic inflammation and it was subsequently found that AngII promoted RAW 264.7 macrophage polarization towards the M1-type by such effects as the release of inducible nitric oxide synthase (iNOS), tumour necrosis factor (TNF)-α, il-1β, the secretion of IL-6, and the expression of M1-type indicators, such as CD86. Simultaneously, compared with the control group, the protein expression levels of Cx43 and phosphorylated (p)-p65 were significantly increased following AngII treatment. The M1-related phenotypic indicators, iNOS, TNF-α, il-1β, IL-6 and CD86, were inhibited by the NF-κB (p65) signalling pathway inhibitor BAY117082. Similarly, the Cx43 inhibitors, Gap26 and Gap19, also inhibited the expression of M1-related factors, and the protein expression levels of p-p65 in the Gap26/Gap19 groups were significantly decreased compared with the AngII group. Altogether, these findings suggested that AngII may induce the polarization of RAW264.7 macrophages to the M1-type through the Cx43/NF-κB (p65) signalling pathway.

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5-Bromo-2-hydroxy-4-methyl-benzaldehyde inhibited LPS-induced production of pro-inflammatory mediators through the inactivation of ERK, p38, and NF-κB pathways in RAW 264.7 macrophages

Cited by 30 publications

References 31 publications

Anti-inflammatory effect of ozonated krill (Euphausia superba) oil in lipopolysaccharide-stimulated RAW 264.7 macrophages

Anti-inflammatory effect of ozonated krill (Euphausia superba) oil in lipopolysaccharide-stimulated RAW 264.7 macrophages

The protective effects of PCPA against monocrotaline-induced pulmonary arterial hypertension are mediated through the downregulation of NFAT-1 and NF-κB

Angiotensin II induces RAW264.7 macrophage polarization to the M1‑type through the connexin 43/NF‑κB pathway

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