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. 2015 Aug;149(2):481–492.e7. doi: 10.1053/j.gastro.2015.04.015

Figure 3.

Figure 3

CM_128 concentration-dependently inhibits CRAC entry and necrosis (PI uptake). (A) Changes in mouse pancreatic acinar [Ca2+]C induced by thapsigargin (Fura-2 340:380 normalized at 2000 s), showing effect of 1 μmol/L CM_128. (B) Mean (±SEM) [Ca2+]C at 2000 and 3000 s from panel A, showing a marked reduction with 1 μmol/L CM_128 (≥62 cells/group; *P < .001, thapsigargin vs thapsigargin plus CM_128 at 3000 s). (C) CM_128 protected isolated murine pancreatic acinar cells from necrotic cell death pathway activation induced by TLCS (500 μmol/L) (mean ± SEM; ≥3 experiments/group; *P < .001, TLCS vs control; †P < .05, TLCS vs TLCS plus CM_128). (D) Concentration-dependent inhibitory effects of CM_128 on cyclopiazonic acid–induced Ca2+ influx, showing a progressive reduction of the initial rate of Ca2+ entry and plateau with increasing CM_128, with complete inhibition of Ca2+ entry at 10 μmol/L (≥17 cells/group). (E) Concentration-dependent inhibitory effects of CM_128 on the initial rate of Ca2+ entry.