Title : Role of mitochondria ROS generation in ethanol-induced NLRP3 inflammasome activation and cell death in astroglial cells.

Pub. Date : 2014

PMID : 25136295






3 Functional Relationships(s)
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1 Here we show that chronic ethanol treatment increases the co-localization of caspase-1 with GFAP(+) cells, and up-regulates IL-1beta and IL-18 in the frontal medial cortex in WT, but not in TLR4 knockout mice. Ethanol interleukin 1 beta Mus musculus
2 Ethanol, as ATP and LPS treatments, up-regulates NLRP3 expression, and causes caspase-1 cleavage and the release of IL-1beta and IL-18 in astrocytes supernatant. Ethanol interleukin 1 beta Mus musculus
3 Ethanol-induced NLRP3/caspase-1 activation is mediated by mitochondrial (m) reactive oxygen species (ROS) generation because when using a specific mitochondria ROS scavenger, the mito-TEMPO (500 muM) or NLRP3 blocking peptide (4 mug/ml) or a specific caspase-1 inhibitor, Z-YVAD-FMK (10 muM), abrogates mROS release and reduces the up-regulation of IL-1beta and IL-18 induced by ethanol or LPS or ATP. Ethanol interleukin 1 beta Mus musculus