IndraLab

Statements



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"Carbon monoxide negatively regulates NLRP3 inflammasome activation in macrophages."

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"Carbon Monoxide Inhibited NLRP3 Inflammasome Activation of AKI in Septic Rats."

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"In our study, CO inhibited the NLRP3 inflammasome activation and decreased the sepsis induced AKI in rats."

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"In the case of the former, CO released by CORM-3 is proposed to inhibit the activation of the NLRP3 inflammasome in cardiac fibroblasts preventing myocardial apoptosis."

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"To block NLRP3 inflammasome and capase-1, PBMCs were pre-incubated for 20 h at 37 °C, and 5% CO 2 with and without 10 μM of OLT1177 (Olatec Therapeutics) or Pralnacasan (VX740 – Vertex, USA)."

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"In terms of decomposition analysis, the aggregate CO 2 intensity effect decreased AII by 23.15 ton/USD and the aggregate structure effect increased AII by 151.51 ton/USD."

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"Previous studies suggested that NLRP3 inflammasome activity is positively regulated by ROS [XREF_BIBR, XREF_BIBR], so CO may inhibit NLRP3 inflammasome activation by decreasing ROS levels in kidney of sepsis induced AKI."

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"CO inhibits the production of IL-1beta induced by inflammasomes and suppresses the activation of the NLRP3 inflammasome in bone marrow derived macrophages; furthermore, CO inhibits mtROS generation, preserves the integrity of mitochondrial membrane, and prevents mtDNA translocation into cytosol."

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"Therefore, CO may also inhibit NLRP3 inflammasome activation by increasing NO levels in sepsis induced AKI."

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"The present study provides a basis for the use of CORM-2 as an effective strategy to protect against sepsis induced AKI, and exogenous CO as released by CORM-2 treatment decreases the oxidative stress and NLRP3 inflammasome activation."

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"Exogenous Carbon Monoxide Decreases Sepsis Induced Acute Kidney Injury and Inhibits NLRP3 Inflammasome Activation in Rats."

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"CO also inhibits NLRP3 inflammasome activation XREF_BIBR, XREF_BIBR, XREF_BIBR, XREF_BIBR."

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"Different CO-releasing molecules or exposure to inhaled CO suppressed NLRP3 inflammasome [69–71], possibly by inducing pyrin production which is its negative regulator [72]."

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"Taken together, these findings indicate that CORM3, and potentially inhalable CO, inhibits activation of the NLRP1 and NLRP3 inflammasomes."

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"Our results suggest that CO negatively regulates NLRP3 inflammasome activation by preventing mitochondrial dysfunction."

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"However, exogenous CO negatively regulates the activation of the NALP3 inflammasome by preventing mitochondrial dysfunction [166], suggesting an anti-inflammatory effect of CO. Exogenous CO also binds to the hemoglobin site on oxidase in macrophage mitochondria, causing a rapid and transient burst of ROS."

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"CO administration by treatment with the CO donor molecule CORM2 (tricarbonyldichlororuthenium (II)) suppressed NLRP3 inflammasome activation in the human monocytic cell line THP-1 [XREF_BIBR], while treatment with the donor CORM3 (tricarbonylchloro (glycinato) ruthenium) inhibited the activation of caspase-1 and production of mature IL-1beta by the human monocytic cell line U937 in response to endoplasmic reticulum stress [XREF_BIBR]."