IndraLab

Statements



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"More recently, Quingyao et al. assumed that DHA-mediated NLRP3 inflammasome inhibition was due to the blockade of high glucoseinduced TXNIP via the PI3K/Akt pathway in pre-adipocytes [103] ."

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"Furthermore, DHA was found to inhibit NLRP3 and NLRP1b inflammasome activation triggered by a variety of agonists, implying a broad inhibitory effect and, consequently, inhibiting the IL-1β production."

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"For example, a recent study has shown that EPA and DHA inhibit the NLRP3 inflammasome in macrophages, independently from their enzymatic products."

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"Moreover, DHA also suppressed the formation of NLRP3 inflammasomes (Liang et al., 2020)."

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"To date, only one study has shown that gavage of DHA in high-fat diet fed mice attenuated NLRP3 inflammasome activation and prevented mice from high-fat diet induced insulin resistance at a whole-body level."

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"In remaining consistent with these studies, pro-inflammatory cascades in TLR4/TLR7, Mitogen-Acivated Protein Kinase (MAPK), Jaks/Stats, Src, IRF1/IRF3, NLRP3, cPLA2/PGE2, NF-κB, AP-1, and CREB were ac[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"Moreover, we tested whether EPA and DHA inhibit LDL-induced priming and/or activation of WAT NLRP3 inflammasome ex vivo (secondary hypothesis)."

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"It was previously reported that DHA inhibited NALP3 inflammasome activation in LPS-primed bone-marrow-derived macrophages [34] ."

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"However, DHA could inhibit the NLRP3 inflammasome independently of these metabolites."

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"showed that DHA suppressed NLRP3 inflammasome by inhibiting NF-kappab activation and enhancing autophagy in macrophages."

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"Since long-chain FAs can activate GPR120 and GPR40 [96] and GPR120 is also involved in the anti-inflammatory effects of omega-3 FAs [93], they tested the role of both receptors on DHA induced NLRP3 in[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"In fact, EPA and DHA inhibited the NLRP3 inflammasome in macrophage cell lines as well as in primary human and murine macrophages [74,80]."

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"In vitro models including adipocytes and macrophage, EPA and/or DHA were shown to inhibit nuclear factor-κB and c-Jun N-terminal kinase pathways and the priming and activation of the NLRP3 inflammasome by metabolic and non-metabolic signals (palmitate, LPS, ATP) ."

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"Recently DHA was reported to inhibit NALP3 inflammasome activation in LPS primed bone-marrow-derived macrophages [49]."

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"By extracting peritoneal macrophages, it was verified that DHA inhibited the activation of NALP3 and regulated the transformation of M1 and M2 cells, thereby reducing I/R injury."

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"Interestingly, the ability of EPA and DHA to inhibit NLRP3 inflammasome activation was not dependent upon their enzymatic metabolism to lipid mediators (e.g., resolvins), but was, in part, dependent upon a GPR120 mediated interaction between betaarr2 and NLRP3 [XREF_BIBR]."

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"When extracellular inflammatory stimulation occurs, IκB is phosphorylated, NF-κB cleavage, and then NF-κB dimer is activated and transferred into the nucleus, and the expression of inflammatory genes are up-regulated.It is reported that GPR120 is involved in the inflammatory signaling pathway activated by long-chain fatty acids, while EPA and DHA inhibit the activation of NLRP3 inflammatory bodies by activating GPR120 [22–24]."

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"When EPA and DHA inhibit the activation of NLRP3 inflammasome, β-arrestin-2 as the downstream protein of GPR120, can inhibit the activation of inflammatory factors by binding to NLRP3 [23, 25]."

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"Further analysis demonstrated that EPA and DHA could significantly suppress the inflammation response of the gut and brain by regulating the NLRP3/ASC signal pathway."

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"Since long-chain FAs can activate GPR120 and GPR40 [96] and GPR120 is also involved in the anti-inflammatory effects of ω-3 FAs [93] , they tested the role of both receptors on DHA-induced NLRP3 in[MISSING/INVALID CREDENTIALS: limited to 200 char for Elsevier]"

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"XREF_BIBR, XREF_BIBR Remarkably, both the NLRP3 inflammasome and mTORC1 are activated by palmitic acid and inhibited by DHA, respectively."