Argon´s cytoprotective properties are mediated via the phosphorylation of ERK1/2, which directly depends on TLR2 and TLR4 signalling.

<p><b>(A)</b> Representative dot-plots of the particular intervention. <b>(B)</b> Annexin V positive and PI negative cells [%] of rotenone-induced apoptosis, consecutive argon treatment and inhibition of ERK1/2 using FR180204 (n = 8; mean±SD; rotenone 11.3±3.3% vs. rotenone+argon 75 Vol% [2 h] 13.1±2.6% and rotenone+argon 75 Vol% [2 h] 13.1±2.6% vs. FR180204+rotenone+argon 75 Vol% [2 h] 21.2±1.9%; both *** = p<0.001) <b>(C)</b> Densitometric analysis and representative Western blot image, demonstrating the phosphorylation of ERK1/2 protein expression after treatment with rotenone, argon and inhibitors of ERK, TLR2 and TLR4. Equal loading was confirmed by reprobing with the non-phosphorylated protein form (t-ERK; n = 8; mean±SD; untreated 0.31±0.07 vs. rotenone 0.66±0.11, rotenone 0.66±0.11 vs. argon 75 Vol% [2 h] 0.42±0.06 and rotenone 0.66±0.11 vs. rotenone+argon 75 Vol% [2 h] 0.93±0.10; all *** = p<0.001; rotenone+argon 75 Vol% [2 h] 0.93±0.10 vs. OxPAPC+rotenone+argon 75 Vol% [2 h] 0.66±0.09; ** = p<0.01 and rotenone+argon 75 Vol% [2 h] 0.93±0.10 vs. TAK-242+rotenone+argon 75 Vol% [2 h] 0.75±0.12, * = p<0.05).