JS-III-49, a hydroquinone derivative, exerts anti-inflammatory activity by targeting Akt and p38

Yi, Young-Su; Kim, Mi‐Yeon; Cho, Jae Youl

doi:10.4196/kjpp.2017.21.3.345

Cited by 4 publications

(3 citation statements)

References 42 publications

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“…The AKT pathway, which is located upstream of the NF-κB pathway, is involved in protein synthesis, proliferation, and survival throughout the process ( Nennig and Schank, 2017 ; Yi et al, 2017 ). The majority of proteins in the NF-κB pathway can regulate inflammation, stress response, and the immune system.…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Prim-O-Glucosylcimifugin on Ulcerative Colitis and Its Mechanism

Yin

Liu

2022

Front. Pharmacol.

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Intestinal epithelial immune dysfunction or imbalance in the homeostasis of intestinal flora can lead to the occurrence or exacerbation of ulcerative colitis (UC). Prim-O-glucosylcimifugin (POG) is an extract of Chinese traditional medicine (TCM) Saposhnikov, which has analgesic, anti-inflammatory, and antioxidant effects. The present work discussed how the POG alternated ulcerative colitis (UC) along with its underlying mechanism. This was clarified by performing animal studies in a mice model, wherein UC was induced by dextran sulfate sodium (DSS). In vivo studies have found that POG increased clinical score, colonic length, and weight of mice in the ulcerative colitis model. It repaired the pathological injury of an intestinal mucosa within mice while inhibiting the inflammatory factor levels such as IL-1β, TNF-α, and IL-6. Meanwhile, by16SrDNA sequencing analysis, it was found that POG regulated the richness of intestinal microbiota structure and repaired the intestinal immune barrier by upregulating the expression levels of tight junction proteins Occludin, Claudin-3, and ZO-1. To further confirm the above results, we found in in vitro studies that POG also protected lipopolysaccharide- (LPS-) induced RAW264.7 cells. POG dramatically suppressed inflammatory factor production (including TNF-α, IL-1β, and IL-6) within LPS-treated RAW264.7 cells by inhibiting the activation of ERK1/2, AKT, JNK1/2, IκB-α, P38, and P65 phosphorylation. In conclusion, POG plays a protective role against UC by inhibiting the activation of pro-inflammatory signaling pathways MAPK, AKT, and NF-κB; repairing the integrity of the intestinal barrier; and regulating the diversity and abundance of intestinal flora.

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Section: Discussionmentioning

confidence: 99%

Protective Effect of Prim-O-Glucosylcimifugin on Ulcerative Colitis and Its Mechanism

Yin

Liu

2022

Front. Pharmacol.

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“…We finally investigated the effect of CK on AKT1-induced inflammatory gene expression. IL-1β and TNF-α are well-known proinflammatory cytokines [4], [6], [45]; therefore, we examined the effect of CK on their mRNA expression by quantitative real-time PCR. CK significantly suppressed the mRNA expression of IL-1β (Fig.…”

Section: Resultsmentioning

confidence: 99%

Compound K, a ginsenoside metabolite, plays an antiinflammatory role in macrophages by targeting the AKT1-mediated signaling pathway

Lee

Choi

Shin

et al. 2019

Journal of Ginseng Research

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BackgroundCompound K (CK) is an active metabolite of ginseng saponin, ginsenoside Rb1, that has been shown to have ameliorative properties in various diseases. However, its role in inflammation and the underlying mechanisms are poorly understood. In this report, the antiinflammatory role of CK was investigated in macrophage-like cells.MethodsThe CK-mediated antiinflammatory mechanism was explored in RAW264.7 and HEK293 cells that were activated by lipopolysaccharide (LPS) or exhibited overexpression of known activation proteins. The mRNA levels of inflammatory genes and the activation levels of target proteins were identified by quantitative and semiquantitative reverse transcription polymerase chain reaction and Western blot analysis.ResultsCK significantly inhibited the mRNA expression of inducible nitric oxide synthase and tumor necrosis factor-α and morphological changes in LPS-activated RAW264.7 cells under noncytotoxic concentrations. CK downregulated the phosphorylation of AKT1, but not AKT2, in LPS-activated RAW264.7 cells. Similarly, CK reduced the AKT1 overexpression-induced expression of aldehyde oxidase 1, interleukin-1β, interferon-β, and tumor necrosis factor-α in a dose-dependent manner.ConclusionOur results suggest that CK plays an antiinflammatory role during macrophage-mediated inflammatory actions by specifically targeting the AKT1-mediated signaling pathway.

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“…The in vitro effects of Ta-EE on the activities of purified target kinases (Syk, Src, and IRAK4) were determined using the kinase profiler service of Millipore (Billerica, MA, USA) as reported previously [ 52 ]. Briefly, each kinase was incubated with reaction buffer containing MgATP for 40 min at room temperature and further incubated after adding 3% phosphoric acid solution to the reaction solution.…”

Section: Methodsmentioning

confidence: 99%

Tabetri™ (Tabebuia avellanedae Ethanol Extract) Ameliorates Osteoarthritis Symptoms Induced by Monoiodoacetate through Its Anti-Inflammatory and Chondroprotective Activities

Park

Hong

et al. 2017

Mediators of Inflammation

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Although osteoarthritis (OA), a degenerative joint disease characterized by the degradation of joint articular cartilage and subchondral bones, is generally regarded as a degenerative rather than inflammatory disease, recent studies have indicated the involvement of inflammation in OA pathogenesis. Tabebuia avellanedae has long been used to treat various diseases; however, its role in inflammatory response and the underlying molecular mechanisms remain poorly understood. In this study, the pharmacological effects of Tabetri (Tabebuia avellanedae ethanol extract (Ta-EE)) on OA pathogenesis induced by monoiodoacetate (MIA) and the underlying mechanisms were investigated using experiments with a rat model and in vitro cellular models. In the animal model, Ta-EE significantly ameliorated OA symptoms and reduced the serum levels of inflammatory mediators and proinflammatory cytokines without any toxicity. The anti-inflammatory activity of Ta-EE was further confirmed in a macrophage-like cell line (RAW264.7). Ta-EE dramatically suppressed the production and mRNA expressions of inflammatory mediators and proinflammatory cytokines in lipopolysaccharide-stimulated RAW264.7 cells without any cytotoxicity. Finally, the chondroprotective effect of Ta-EE was examined in a chondrosarcoma cell line (SW1353). Ta-EE markedly suppressed the mRNA expression of matrix metalloproteinase genes. The anti-inflammatory and chondroprotective activities of Ta-EE were attributed to the targeting of the nuclear factor-kappa B (NF-κB) and activator protein-1 (AP-1) signaling pathways in macrophages and chondrocytes.

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JS-III-49, a hydroquinone derivative, exerts anti-inflammatory activity by targeting Akt and p38

Cited by 4 publications

References 42 publications

Protective Effect of Prim-O-Glucosylcimifugin on Ulcerative Colitis and Its Mechanism

Protective Effect of Prim-O-Glucosylcimifugin on Ulcerative Colitis and Its Mechanism

Compound K, a ginsenoside metabolite, plays an antiinflammatory role in macrophages by targeting the AKT1-mediated signaling pathway

Tabetri™ (Tabebuia avellanedae Ethanol Extract) Ameliorates Osteoarthritis Symptoms Induced by Monoiodoacetate through Its Anti-Inflammatory and Chondroprotective Activities

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