Fulgidic Acid Isolated from the Rhizomes of &lt;i&gt;Cyperus rotundus&lt;/i&gt; Suppresses LPS-Induced iNOS, COX-2, TNF-α, and IL-6 Expression by AP-1 Inactivation in RAW264.7 Macrophages

Shin, Ji‐Sun; Hong, Yujin; Lee, Hwi-Ho; Ryu, Byeol; Cho, Young-Wuk; Kim, Nam‐Jung; Jang, Dae Sik; Lee, Kyung‐Tae

doi:10.1248/bpb.b15-00186

Cited by 40 publications

(23 citation statements)

References 29 publications

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“…In rat NP cells, CCAAT/enhancer binding protein β (C/EBPβ) increases the levels of TNF-α, which is mediated by the extracellular signalregulated kinase 1/2 (ERK1/2) and p38 mitogen activated protein kinase (MAPK) pathways [19]. In monocytes and macrophages, lipopolysaccharide (LPS) induces TNF-α expression by activating early growth response factor-1 (Egr-1) [20], activator protein-1 (AP-1) [21], MAPK [22], and nuclear factor-κB (NF-κB) [23]. In neonatal rat cardiac fibroblasts, the activating transcription factor-2 (ATF-2)/c-Jun signaling pathway, but not NF-κB, is required for the up-regulation of TNF-α expression induced by angiotensin II and LPS [24].…”

Section: Structure and Synthesis Of Tnf-αmentioning

confidence: 99%

“…NF-κB is thus released and then rapidly enters the nucleus to trigger transcription of multiple target genes, including cytokines, chemokines, matrix metalloproteinases (MMPs), a disintegrin and metalloprotease with thrombospondin motifs (ADAMTSs), and pro-survival genes [41,42]. Interestingly, NF-κB is also able to stimulate TNF-α production [21], thereby providing a positive feedback loop between both factors to further amplify the biological effects of TNF-α.…”

Section: Tnfr1-dependent Signaling Pathwaysmentioning

confidence: 99%

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Tumor necrosis factor-α: a key contributor to intervertebral disc degeneration

Wang¹,

Yu²,

Yan³

et al. 2017

ABBS

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Intervertebral disc (IVD) degeneration (IDD) is the most common cause leading to low back pain (LBP), which is a highly prevalent, costly, and crippling condition worldwide. Current treatments for IDD are limited to treat the symptoms and do not target the pathophysiology. Tumor necrosis factor-α (TNF-α) is one of the most potent pro-inflammatory cytokines and signals through its receptors TNFR1 and TNFR2. TNF-α is highly expressed in degenerative IVD tissues, and it is deeply involved in multiple pathological processes of disc degeneration, including matrix destruction, inflammatory responses, apoptosis, autophagy, and cell proliferation. Importantly, anti-TNF-α therapy has shown promise for mitigating disc degeneration and relieving LBP. In this review, following a brief description of TNF-α signal transduction, we mainly focus on the expression pattern and roles of TNF-α in IDD, and summarize the emerging progress regarding its inhibition as a promising biological therapeutic approach to disc degeneration and associated LBP. A better understanding will help to develop novel TNF-α-centered therapeutic interventions for degenerative disc disease.

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Section: Structure and Synthesis Of Tnf-αmentioning

confidence: 99%

Section: Tnfr1-dependent Signaling Pathwaysmentioning

confidence: 99%

Tumor necrosis factor-α: a key contributor to intervertebral disc degeneration

Wang¹,

Yu²,

Yan³

et al. 2017

ABBS

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show abstract

“…In addition to 14,15-EET, the growth of dormant micrometastases might also be triggered by other factors through similar mechanisms. For example, infection could induce the production of G-CSF/IL-6 and PGE 2 [46]. PGE 2 could induce the expression of CXCL1 in tumor cells [47].…”

Section: Discussionmentioning

confidence: 99%

14,15-EET induces the infiltration and tumor-promoting function of neutrophils to trigger the growth of minimal dormant metastases

et al. 2016

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Infiltrating neutrophils are known to promote in thedevelopment of tumor. However, it is unclear whether and how neutrophils areinvolved in triggering the growth of dormant metastases. Here we show that14,15-epoxyeicosatrienoic acid (14,15-EET) can trigger the growth of dormantmicrometastases by inducing neutrophilic infiltration and converting neutrophilfunction. 14,15-EET triggered neutrophil infiltration in metastatic lesions byactivating STAT3 and JNK pathways to induce the expression of human IL-8 andmurine CXCL15 in corresponding tumor cells. The continuous expression ofhIL-8/mCXCL15 was maintained by the sustained and enhanced activation of JNKpathway. 14,15-EET up-regulated miR-155 expression by activating STAT3 and JNKpathways. miR-155 in turn down-regulated the expression of SHIP1 and DET1, thusaugmenting the activation of JNK and c-Jun. Moreover, the function ofneutrophils was converted from tumor-suppressing to tumor-promoting by14,15-EET in vivo. By inducing the production of G-CSF/IL-6 in vivo, 14,15-EET induced the enhancement of STAT3 activation in neutrophilsto increase MMP-9 expression and decrease TRAIL expression. Neutrophil-derivedMMP-9 was required for 14,15-EET to induce angiogenesis during the growth ofdormant micrometastases. Depleting neutrophils or inhibiting hIL-8/mCXCL15up-regulation resulted in the failure of 14,15-EET to promote the developmentof micrometastases. These findings reveal a mechanism through which theinfiltration and tumor-promoting function of neutrophils could be induced totrigger the growth of dormant metastases, which might be a driving force forthe tumor recurrence based on dormant metastases.

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“…RAW246,7 makrofágokon végzett kísérletek alapján kimutatták, hogy a fulgidsav gátolja az LPS-indukált TNF-α-, IL-6-és PGE 2 -expressziót, valamint a NO-képződést az AP-1 transzkripciós faktor inaktivációján keresztül [15].…”

Section: Az Elhízás Kezelése Az áJurvédábanunclassified

Ájurvéda az elhízás kezelésében

Korossy

Blázovics

2016

Orvosi Hetilap

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Az életmód változásával és a gyorséttermi láncok elterjedésével egyre nagyobb problémát jelent az elhízás az egész világon. Indiában a férfiak 31%-a, a nők 29%-a túlsúlyos, és az elhízás az utóbbi 11 évben növekvő tendenciát mutat. Az elhízás növeli számos betegség kialakulásának esélyét, mint például a szív-és érrendszeri betegségek, refluxbetegség, gastrointestinalis tumorok és alvási apnoe. Műtétek során a szövődményekkel még nem járó elhízás is súlyos komplikációkat okozhat. Az Ájurvédában a betegségek kialakulásáért a 3 dosha -vata, pitta, kapha -egyensúlyának felborulása a felelős. A 3 dosha aránya egyénenként változik, és meghatározza az egyéni testalkatot. Egy indiai kutatócsoport kimutatta, hogy az ájurvédikus testtípus-besorolás kapcsolatba hozható a gyulladásos és oxidatívstressz-faktorok génjeivel, a DNS-metilációval és a cardiovascularis betegségek kialakulásának esélyeivel. Orv. Hetil., 2016, 157(34), 1349-1352. Kulcsszavak: Ájurvéda, elhízás, dyslipidaemia, testtípus, DNS-metiláció Ayurveda for the treatment of obesityObesity is an increasing problem all over the world as the lifestyle changes and fast food chains gain popularity. In India, 31% of men and 29% of women are overweight, which is a growing trend over the last 11 years. Obesity increases the risk of many diseases such as cardiovascular diseases, reflux disease, gastrointestinal tumors, and sleep apnea. Obesity without complications can also cause serious complications during surgery. In Ayurveda the formation of diseases depends on the balance of the three doshas -vata, pitta, kapha. The rate of three doshas varies depending on the body constitution of the indvidual. Studies of an Indian research group have shown that Ayurvedic body type classification may be associated with genes of inflammation and oxidative stress factors, the rate of DNA methylation and development of cardiovascular diseases. Rövidítések AMP = adenozin-monofoszfát; AP-1 = activator protein-1; BMI = (body mass index) testtömegindex; CoA = koenzim-A; COX-2 = ciklooxigenáz-2; DNS = dezoxiribonukleinsav; FPG = (fasting plasma glucose concentration) éhomi plazmaglükóz-koncentráció; HDL = (high density lipoprotein) magas sűrűségű lipoprotein; HLA = humán leukocyta-antigén; HOMA-IR = homeostatic model assessment of insulin resistance; hs-CRP = (high sensitive C-reactive protein) magas ér-zékenységű C-reaktív protein; IL-1β = interleukin-1-β; IL-6 = interleukin-6; iNOS = indukálható nitrogén-monoxid-szintáz; LDL = (low density lipoprotein) alacsony sűrűségű lipoprotein; LPS = lipopoliszacharid; mRNS = messenger ribonukleinsav; NO = nitrogén-monoxid; PGE 2 = prosztaglandin E 2 ; SNP = single nucleotide polymorphism; TG = triglicerid; TNF-α = tumornekrózis-faktor-α; WHO = World Health Organization Keywords India és az elhízásAz életmód változásával és a különböző gyorséttermi láncok térhódításának köszönhetően az egész világon egyre nagyobb jelentőséggel bír az obesitas leküzdése. A WHO 2015-ös statisztikája szerint Indiában a férfiak 31%-a, a nők 29%-a túlsúlyos, s ez növe...

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Fulgidic Acid Isolated from the Rhizomes of <i>Cyperus rotundus</i> Suppresses LPS-Induced iNOS, COX-2, TNF-α, and IL-6 Expression by AP-1 Inactivation in RAW264.7 Macrophages

Cited by 40 publications

References 29 publications

Tumor necrosis factor-α: a key contributor to intervertebral disc degeneration

Tumor necrosis factor-α: a key contributor to intervertebral disc degeneration

14,15-EET induces the infiltration and tumor-promoting function of neutrophils to trigger the growth of minimal dormant metastases

Ájurvéda az elhízás kezelésében

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Fulgidic Acid Isolated from the Rhizomes of <i>Cyperus rotundus</i> Suppresses LPS-Induced iNOS, COX-2, TNF-α, and IL-6 Expression by AP-1 Inactivation in RAW264.7 Macrophages

Cited by 40 publications

References 29 publications

Tumor necrosis factor-&alpha;: a key contributor to intervertebral disc degeneration

Tumor necrosis factor-&alpha;: a key contributor to intervertebral disc degeneration

14,15-EET induces the infiltration and tumor-promoting function of neutrophils to trigger the growth of minimal dormant metastases

Ájurvéda az elhízás kezelésében

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Tumor necrosis factor-α: a key contributor to intervertebral disc degeneration

Tumor necrosis factor-α: a key contributor to intervertebral disc degeneration