Figure 8. Allicin inhibits the activation of TRAF6/MAPK/NF-κB and STAT3/NF-κB signaling pathways in the IL-17A-stimulated HaCaT cells. (A) The protein expression of TRAF6, p38, phospho-p38, JNK, phospho-JNK, Erk1/2, phospho-Erk1/2, STAT3, phospho-STAT3, p65, and phospho-p65 in HaCaT cells stimulated with IL17A at indicated time points were measured by western blotting. β-actin was used as a loading control. (B, C) HaCaT cells were pretreated with 12.8ug/ml allicin for 7.5h and subsequently stimulated with IL-17A (25 ng/ml) for an additional 0.5h. Western blot showing the protein expression of TRAF6, P38, phospho-P38, JNK, phospho-JNK, ERK1/2, phospho-ERK1/2, STAT3, phospho-STAT3, P65, and phospho-P65 in HaCaT cells (n=3). (D, E) Western blot showing the protein expression of TRAF6, P38, phospho-P38, JNK, phospho-JNK, ERK1/2, phospho-ERK1/2, STAT3, phospho-STAT3, P65, and phospho-P65 in IMQ-induced psoriasis-like lesions treated with or without allicin (n=5). (F) Putative pathway for allicin-mediated regulation of inflammation and hyperproliferation in IMQ-induced psoriatic lesions. Data are expressed as means ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.