Title : Astragaloside IV Suppresses High Glucose-Induced NLRP3 Inflammasome Activation by Inhibiting TLR4/NF-κB and CaSR.

Pub. Date : 2019

PMID : 30906223






5 Functional Relationships(s)
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1 Astragaloside IV Suppresses High Glucose-Induced NLRP3 Inflammasome Activation by Inhibiting TLR4/NF-kappaB and CaSR. Glucose NLR family pyrin domain containing 3 Homo sapiens
2 The results showed that high glucose increased the expression of interleukin-18 (IL-18), interleukin-1beta (IL-1beta), NLRP3, caspase-1, and ASC, as well as the protein level of TLR4, nucleus p65, and CaSR. Glucose NLR family pyrin domain containing 3 Homo sapiens
3 Meanwhile, NPS2143, BAY 11-7082, and INF39 could significantly abolish the high glucose-enhanced NLRP3, ASC, caspase-1, IL-18, and IL-1beta expression in vitro. Glucose NLR family pyrin domain containing 3 Homo sapiens
4 In addition, both NPS2143 and BAY 11-7082 attenuated high glucose-induced upregulation of NLRP3, ASC, caspase-1, IL-18, and IL-1beta expression. Glucose NLR family pyrin domain containing 3 Homo sapiens
5 In conclusion, this study suggested that As-IV could inhibit high glucose-induced NLRP3 inflammasome activation and subsequent secretion of proinflammatory cytokines via inhibiting TLR4/NF-kappaB signaling pathway and CaSR, which provides new insights into the anti-inflammatory activity of As-IV. Glucose NLR family pyrin domain containing 3 Homo sapiens