β-AR blockers protected cardiomyocytes against ER stress-mediated apoptosis.

Abstract

<p>(A) β-AR blockers suppressed activation of caspase-12 in H9c2(2–1) cells. Cells were treated with TG (5 µmol/L) or TM (5 µg/ml) with or without metoprolol (10 µmol/L) or propranolol (10 µmol/L) for 12 hours. Cell lysates were then immunoblotted for caspase-12. Caspase-12 cleavage was normalized to β-actin. *P<0.05 vs. control, #P<0.05 vs. TM, & P<0.05 vs. TG. (B) and (C) Hochst-positive cells (%). H9c(2–1) cells were pretreated with metoprolol (10 µmol/L, 1 h) or propranolol (10 µmol/L, 1 h), then exposed to TG (5 µmol/L, 24 h) or TM (5 µg/ml, 24 h) before staining with Hochst33258 as indicated. Hochst-positive cells are expressed as a percentage of the number of total cells. **P<0.001 vs. control. # P<0.05 vs. TG or TM. (D) Anexin V-positive cells (%). H9c(2–1) cells were pretreated with metoprolol (10 µmol/L, 1 h) or propranolol (10 µmol/L, 1 h), then exposed to TG (5 µmol/L, 24 h) before staining with Anexin V/PI as indicated. Analyze by flow cytometry immediately after incubation. Anexin V-positive cells are expressed as a percentage of the number of total cells. *P<0.05 vs. control. #P<0.05 vs. TG.</p

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