Figure 7.

β-arr1 ameliorated chemotherapy-induced intestinal apoptosis by downregulating ER stress-mediated mitochondrial apoptotic signaling. (a) Expression of GRP78 and cleaved caspase-12 protein was analyzed by western blotting, and β-actin was used as the loading control. Three independent experiments were performed. (b) Intestinal sections were stained for GRP78. (c) Intestinal sections were stained for cleaved caspase-12. (d) GRP78, caspase-12, caspase-9 and caspase-3 were examined in HCT116 cells following the indicated treatments by western blotting, and β-actin was used as the loading control. Veh, vehicle; Vec, vector. Three independent experiments were performed. (e) After 5-FU administration, HCT116 cells overexpressing β-arr1 were stained for caspase-3 (red). (f) The apoptotic index was determined in the cells following 5-FU administration. Values are shown as the mean±S.D. Three independent experiments were performed. (g) Bax, Bak and cytochrome c levels were determined in both mitochondrial and cytosolic fractions by western blotting, and β-actin and Cox IV were markers of cytosolic and mitochondrial fractions, respectively. Three independent experiments were performed