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Methane and Inflammation - A Review (Fight Fire with Fire)

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Figure

Table 1 Summary of in vivo studies using CH4 that also monitored sepsis/LPS/surgery-inducedorgan dysfunction and other parameters of tissue damage
Fig. 1 Documented CHinflammation. ATF4, activating transcription factor 4; Bax. Bcl-2-associated X protein; Bcl-2, B cell lymphoma 2; CHOP,C/EBP homologous protein; CLP, cecal ligation and puncture; CNS, central nervous system; CytC, cytochrome C; ENS,enteric nervous system; ER, endoplasmic reticulum; GRP78, glucose-regulated protein 78; GSK-3kinase 3 beta; GSH, glutathione; GSSG, glutathione disulphide; HO-1, heme oxygenase 1; IL-1IL-10, interleukin 6 and interleukin 10, respectively; I/R, ischemia/reperfusion; LPS, lipopolysaccharide; MAPKs,mitogen-activated protein kinase; MPO, myeloperoxidase; NF-3; PARP, poly (ADP-ribose) polymerase; PPAR-oxygen species; SOD, superoxide dismutase; TLR4, Toll-like receptor 4; TNF-4-mediated mechanisms in experimental models of sepsis, endotoxemia and systemicβ, glycogen synthaseβ, interleukin 1 beta; IL-6,κB, nuclear factor-κB; NLRP3, NOD-like receptor proteinγ, peroxisome proliferator-activated receptor gamma; ROS, reactiveα, tumour necrosis factor alpha; XOR,xanthine oxidoreductase

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