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article, google, scholar, cas, liu, journal, wang, signaling, zhang, cells, pathway, yang, research, tlr, neuroinflammation, microglia, tlrinc, attenuates, kim, inflammatory, international, nlrp, brain, lee, responses, microglial, inhibiting, sciences, ros, yuehua, lps, effects, activity, tolllike, huang, receptor, medical, privacy, cookies, content, data, information, downregulating, generation, shanshan, guanhua, antineuroinflammatory, access, inflammasome, activation,

Topics {✒️}

tlr4/myd88/nf-κb/nlrp3 signaling pathway ros/nlrp3/caspase-1/il-1β signaling pathway tlr4/myd88/nf-κb signaling pathway akt/nf-kb-inflammatory signaling pathways inhibiting hsp70-tlr4-nlrp3-mediated neuroinflammation inhibiting nlrp3/caspase-1/il-1β axis ffa/tlr4/nf-κb axis guan-hua du designed yue-hua wang analyzed regulating tlr4/myd88 pathway month download article/chapter guan-hua du yue-hua wang akt nf-κb lps-stimulated bv2 cells nrf2/ho-1 signaling pathways hypoxia/reoxygenation-induced injury mg53 protects huc-mscs lipopolysaccharide-activated bv2 microglia tlr4/nf-κb lps-treated bv2 cells inhibiting nf-κb stz-induced diabetic mice high-fat-diet rats tlr4 signaling pathway inactivating nf-κb age-linked neurodegenerative diseases lps-activated mouse microglia low-molecular weight polysaccharide disease-inducing mechanisms resulting lps-activated bv2 microglia induced inflammatory responses microglial bv2 cells bv2 microglial cells nlrp3 inflammasome activation 5-induced microglial polarization related subjects article inflammation aims synthetic tlr4 antagonist complement signaling pathways central nervous system piperine attenuates lipopolysaccharide inhibiting nlrp3 transcription lps-stimulated mice ying-lin yang performed nf-κb full article pdf anti-neuroinflammatory response privacy choices/manage cookies hispidulin inhibits neuroinflammation

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         headline:TLR4-IN-C34 Inhibits Lipopolysaccharide-Stimulated Inflammatory Responses via Downregulating TLR4/MyD88/NF-κB/NLRP3 Signaling Pathway and Reducing ROS Generation in BV2 Cells
         description:TLR4 signal activated by lipopolysaccharide (LPS) is involved in the pathological process of the central nervous system (CNS) diseases and the suppression of TLR4 signal may become an effective treatment. TLR4-IN-C34, a TLR4 inhibitor, is expected to become a candidate compound with anti-neuroinflammatory response. In the present study, the anti-neuroinflammatory effects and possible mechanism of TLR4-IN-C34 were investigated in BV2 microglia cells stimulated by LPS. The results showed that TLR4-IN-C34 decreased the levels of pro-inflammatory factors and chemokines including NO, TNF-α, IL-1β, IL-6, and MCP-1 in the supernatant of LPS-stimulated BV2 cells. Further research indicated that TLR4-IN-C34 suppressed the expression or phosphorylation levels of inflammatory proteins regarding TLR4/MyD88/NF-κB/NLRP3 signaling pathway. In addition, TLR4-IN-C34 reduced ROS production in BV2 cells after LPS treatment. In conclusion, our findings suggest that anti-neuroinflammatory activity of TLR4-IN-C34 may be interrelated to the inhibition of TLR4/MyD88/NF-κB/NLRP3 signaling pathway and reduction of ROS generation.
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      description:TLR4 signal activated by lipopolysaccharide (LPS) is involved in the pathological process of the central nervous system (CNS) diseases and the suppression of TLR4 signal may become an effective treatment. TLR4-IN-C34, a TLR4 inhibitor, is expected to become a candidate compound with anti-neuroinflammatory response. In the present study, the anti-neuroinflammatory effects and possible mechanism of TLR4-IN-C34 were investigated in BV2 microglia cells stimulated by LPS. The results showed that TLR4-IN-C34 decreased the levels of pro-inflammatory factors and chemokines including NO, TNF-α, IL-1β, IL-6, and MCP-1 in the supernatant of LPS-stimulated BV2 cells. Further research indicated that TLR4-IN-C34 suppressed the expression or phosphorylation levels of inflammatory proteins regarding TLR4/MyD88/NF-κB/NLRP3 signaling pathway. In addition, TLR4-IN-C34 reduced ROS production in BV2 cells after LPS treatment. In conclusion, our findings suggest that anti-neuroinflammatory activity of TLR4-IN-C34 may be interrelated to the inhibition of TLR4/MyD88/NF-κB/NLRP3 signaling pathway and reduction of ROS generation.
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      name:State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
      name:Beijing Key Laboratory of Drug Target Identification and New Drug Screening, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
      name:State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
      name:Beijing Key Laboratory of Drug Target Identification and New Drug Screening, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
      name:State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
      name:Beijing Key Laboratory of Drug Target Identification and New Drug Screening, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
      name:State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
      name:Beijing Key Laboratory of Drug Target Identification and New Drug Screening, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
      name:State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
      name:Beijing Key Laboratory of Drug Target Identification and New Drug Screening, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
      name:State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
      name:Beijing Key Laboratory of Drug Target Identification and New Drug Screening, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
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