2019
DOI: 10.1016/j.intimp.2019.105754
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The role of inflammasome activation in Triptolide-induced acute liver toxicity

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Cited by 34 publications
(19 citation statements)
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“…And caspase-1 inhibitor (Ac-Yvad-Cmk) pretreatment effectively decreased the recruitment of neutrophils and inhibited the production of massive pro-inflammatory factors (IL-1β, TNF-α, IL-6, and MCP1; Yuan et al, 2019). Those findings suggested that triptolide induced hepatotoxicity mainly through the proinflammatory effects mediated by NLRP3 inflammasome.…”
Section: Triptolide-induced Liver Injurymentioning
confidence: 87%
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“…And caspase-1 inhibitor (Ac-Yvad-Cmk) pretreatment effectively decreased the recruitment of neutrophils and inhibited the production of massive pro-inflammatory factors (IL-1β, TNF-α, IL-6, and MCP1; Yuan et al, 2019). Those findings suggested that triptolide induced hepatotoxicity mainly through the proinflammatory effects mediated by NLRP3 inflammasome.…”
Section: Triptolide-induced Liver Injurymentioning
confidence: 87%
“…Mice treated with a single dose of triptolide (600 µg/kg) displayed liver injury with a time-dependent activation of NLRP3 inflammasome, accompanied by the increase of serum transaminases and elevation of neutrophils infiltration. The activation of TLR4-Myd88-NF-κB pathway and oxidative stress induced by triptolide might be responsible for the activation of NLRP3 inflammasome (Yuan et al, 2019).…”
Section: Triptolide-induced Liver Injurymentioning
confidence: 99%
“…In addition, Fu et al [88] indicated that triptolide administration induced liver injury accompanied by microcystic steatosis, hyperlactatemia and increased oxidative stress, resulting from the inhibition of mitochondrial respiratory chain and secondary β-oxidative damage. Furthermore, Yuan et al [89] suggested oxidative stress induced by triptolide might be related to the activation of NLR family pyrin domain containing 3 (NLRP3) inflammasome, which can result in the release of cytokines and recruitment of the inflammatory cells, and further augment the liver damage. Besides, Wang et al [90] showed that 0.5 mg/kg of triptolide enhanced the expansion of Th17 cells and suppressed the production of Tregs in female C57BL/6 mice, which may represent a new pathogenesis of TPinduced liver injury.…”
Section: Hepatotoxicitymentioning
confidence: 99%
“…However, abnormal accumulation of neutrophils can lead to unexpected injury to host organs including DILI. Recently, more studies have defined that neutrophil activation commonly causes DILI, in which mitochondrial DNA originates from injured hepatocytes that could further activate neutrophils (You et al, 2006;Moles et al, 2014;Williams et al, 2014;Yuan et al, 2019). Liver injury increased expressions of chemokines, cytokines, and other immune molecules that could regulate neutrophil recruitment and activation, which cause cytotoxicity and hepatocyte death (Ramaiah and Jaeschke, 2007).…”
Section: Neutrophilsmentioning
confidence: 99%