IKK<i>β</i>‐Targeted Anti‐Inflammatory Activities of a Butanol Fraction of Artificially Cultivated <i>Cordyceps pruinosa</i> Fruit Bodies

Kim, Han Gyung; Yang, Woo Seok; Sung, Gi‐Ho; Kim, Ji Hye; Baek, Gwang-Soo; Kim, Eunji; Yang, Soo Jin; Park, Yung Chul; Sung, Jae Mo; Yoon, Deok Hyo; Kim, Tae‐Woong; Hong, Sungyoul; Kim, Jong-Hoon; Cho, Jae Youl

doi:10.1155/2014/562467

Cited by 12 publications

(8 citation statements)

References 41 publications

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“…Several studies have shown that translocation of NFκB from the cytoplasm to the nucleus may be crucial for overexpression of inflammatory mediators such as COX-2, iNOS, TNF-α, IL-1β, IL-6, IL-10 and MCP-1 [ 57 ]. The phosphorylation of IκBα and IKKβ is a vital event for NFκB activation [ 58 ]. It is established that activation of ERK may be partially responsible for LPS-induced iNOS and COX-2 expressions in RAW 264.7 macrophages [ 49 , 55 ].…”

Section: Discussionmentioning

confidence: 99%

Vaccaria hypaphorine alleviates lipopolysaccharide-induced inflammation via inactivation of NFκB and ERK pathways in Raw 264.7 cells

Sun

Cai

Wang

et al. 2017

BMC Complement Altern Med

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BackgroundActivation of macrophage is involved in many inflammation diseases. Lipopolysaccharide (LPS) is a powerful inflammatory signal contributing to monocytes/macrophages activation associated with increased proinflammatory cytokines expressions. We recently identified that vaccarin was expected to protect endothelial cells from injury. Hypaphorine was abundantly found in vaccaria semen. However, the potential roles and underlying mechanisms of vaccaria hypaphorine on macrophage inflammation have been poorly defined.MethodsThis study was designed to determine the effects of vaccaria hypaphorine on LPS-mediated inflammation in RAW 264.7 cells.ResultsIn this study, we demonstrated that vaccaria hypaphorine dramatically ameliorated LPS-induced nitric oxide (NO) release and productions of proinflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, IL-10, monocyte chemoattractant protein 1 (MCP-1) and prostaglandin E2 (PGE2) in RAW 264.7 cells. LPS-stimulated expressions of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) were down-regulated by vaccaria hypaphorine. Furthermore, vaccaria hypaphorine retarded LPS-induced phosphorylation of ERK, nuclear factor kappa beta (NFκB), NFκB inhibitor IκBα, and IKKβ. Immunofluorescence staining revealed that vaccaria hypaphorine eliminated the nuclear translocation of NFκB in LPS-treated RAW 264.7 cells.ConclusionIt was seen that vaccaria hypaphorine counteracted inflammation via inhibition of ERK or/and NFκB signaling pathways. Collectively, we concluded that vaccaria hypaphorine can be served as an anti-inflammatory candidate.Electronic supplementary materialThe online version of this article (doi:10.1186/s12906-017-1635-1) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Vaccaria hypaphorine alleviates lipopolysaccharide-induced inflammation via inactivation of NFκB and ERK pathways in Raw 264.7 cells

Sun

Cai

Wang

et al. 2017

BMC Complement Altern Med

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“…All other chemicals were obtained from Sigma Chemical Co. Total or phospho-specific antibodies were purchased from Cell Signaling Technology (Beverly, MA, USA). Plasmid constructs containing AKT, IKKβ, and TBK1 were used as reported previously [24], [25], [26].…”

Section: Methodsmentioning

confidence: 99%

In vitro antioxidative and anti-inflammatory effects of the compound K-rich fraction BIOGF1K, prepared from Panax ginseng

Hossen

Hong

Baek

et al. 2017

Journal of Ginseng Research

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BackgroundBIOGF1K, a compound K-rich fraction prepared from the root of Panax ginseng, is widely used for cosmetic purposes in Korea. We investigated the functional mechanisms of the anti-inflammatory and antioxidative activities of BIOGF1K by discovering target enzymes through various molecular studies.MethodsWe explored the inhibitory mechanisms of BIOGF1K using lipopolysaccharide-mediated inflammatory responses, reporter gene assays involving overexpression of toll-like receptor adaptor molecules, and immunoblotting analysis. We used the 2,2-diphenyl-1-picrylhydrazyl (DPPH) assay to measure the antioxidative activity. We cotransfected adaptor molecules, including the myeloid differentiation primary response gene 88 (MyD88) and Toll/interleukin-receptor domain containing adaptor molecule-inducing interferon-β (TRIF), to measure the activation of nuclear factor (NF)-κB and interferon regulatory factor 3 (IRF3).ResultsBIOGF1K suppressed lipopolysaccharide-triggered NO release in macrophages as well as DPPH-induced electron-donating activity. It also blocked lipopolysaccharide-induced mRNA levels of interferon-β and inducible nitric oxide synthase. Moreover, BIOGF1K diminished the translocation and activation of IRF3 and NF-κB (p50 and p65). This extract inhibited the upregulation of NF-κB-linked luciferase activity provoked by phorbal-12-myristate-13 acetate as well as MyD88, TRIF, and inhibitor of κB (IκBα) kinase (IKKβ), and IRF3-mediated luciferase activity induced by TRIF and TANK-binding kinase 1 (TBK1). Finally, BIOGF1K downregulated the NF-κB pathway by blocking IKKβ and the IRF3 pathway by inhibiting TBK1, according to reporter gene assays, immunoblotting analysis, and an AKT/IKKβ/TBK1 overexpression strategy.ConclusionOverall, our data suggest that the suppression of IKKβ and TBK1, which mediate transcriptional regulation of NF-κB and IRF3, respectively, may contribute to the broad-spectrum inhibitory activity of BIOGF1K.

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“…To further confirm the effects of MPP on transcriptional activation, a luciferase reporter gene activity assay was employed. HEK293 cells were co-transfected with NF-κB-Luc reporter genes under the overexpression of the adaptor molecules TRIF and MyD88, as reported previously [ 25 26 ]. Under these conditions, cells exhibited increased levels of luciferase activity up to 140- and 900-fold in the presence of TRIF and MyD88, respectively ( Figs.…”

Section: Resultsmentioning

confidence: 99%

(E)-3-(3-methoxyphenyl)-1-(2-pyrrolyl)-2-propenone displays suppression of inflammatory responses via inhibition of Src, Syk, and NF-κB

Kim

Jeong

Lee

et al. 2016

Korean J Physiol Pharmacol

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(E)-3-(3-methoxyphenyl)-1-(2-pyrrolyl)-2-propenone (MPP) is an aldol condensation product resulting from pyrrole-2-carbaldehyde and m- and p- substituted acetophenones. However, its biological activity has not yet been evaluated. Since it has been reported that some propenone-type compounds display anti-inflammatory activity, we investigated whether MPP could negatively modulate inflammatory responses. To do this, we employed lipopolysaccharide (LPS)-stimulated macrophage-like RAW264.7 cells and examined the inhibitory levels of nitric oxide (NO) production and transcriptional activation, as well as the target proteins involved in the inflammatory signaling cascade. Interestingly, MPP was found to reduce the production of NO in LPS-treated RAW264.7 cells, without causing cytotoxicity. Moreover, this compound suppressed the mRNA levels of inflammatory genes, such as inducible NO synthase (iNOS) and tumor necrosis factor (TNF)-α. Using luciferase reporter gene assays performed in HEK293 cells and immunoblotting analysis with nuclear protein fractions, we determined that MPP reduced the transcriptional activation of nuclear factor (NF)-κB. Furthermore, the activation of a series of upstream signals for NF-κB activation, composed of Src, Syk, Akt, and IκBα, were also blocked by this compound. It was confirmed that MPP was able to suppress autophosphorylation of overexpressed Src and Syk in HEK293 cells. Therefore, these results suggest that MPP can function as an anti-inflammatory drug with NF-κB inhibitory properties via the suppression of Src and Syk.

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IKKβ‐Targeted Anti‐Inflammatory Activities of a Butanol Fraction of Artificially Cultivated Cordyceps pruinosa Fruit Bodies

Cited by 12 publications

References 41 publications

Vaccaria hypaphorine alleviates lipopolysaccharide-induced inflammation via inactivation of NFκB and ERK pathways in Raw 264.7 cells

Vaccaria hypaphorine alleviates lipopolysaccharide-induced inflammation via inactivation of NFκB and ERK pathways in Raw 264.7 cells

In vitro antioxidative and anti-inflammatory effects of the compound K-rich fraction BIOGF1K, prepared from Panax ginseng

(E)-3-(3-methoxyphenyl)-1-(2-pyrrolyl)-2-propenone displays suppression of inflammatory responses via inhibition of Src, Syk, and NF-κB

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