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. 2014 Jan 31;47(2):161–171. doi: 10.1111/cpr.12091

Figure 6.

Figure 6

Rapamycin ( Rap ) specifically inhibited acrolein ( Acr )‐induced apoptosis. Cells were exposed to 100 μm Acr‐stimulated apoptosis for 12 h through activation of GPCR, PKG and EGFR‐ERK pathways, and determined by FITC‐labelled annexin V/PI apoptosis kit, with or without pre‐treatment with Rap (0.1 μm Rap), SB (50 μm SB203580), PDTC (20 μm Ammonium pyrrolidinedithiocarbamate), PD98 (50 μm PD98059) and H89 (20 μm H‐89·2HCl), which are inhibitors of mTOR, P38, NF‐κB, MAPKK and PKA, respectively (a and b). Only Rap specifically inhibited Acr‐induced apoptosis. There were no significant effect of inhibition of Acr‐induced apoptosis by other inhibitors. *P < 0.05, compared to 100 μm Acr marked as control group.