Objectives To investigate the effect of endoplasmic reticulum stress (ERS) in the process of advanced glycosylation end products (AGEs)-induced neonatal rat cardiomyocyte apoptosis.
Methods Cultured neonatal rat cardiomyocytes were randomly divided into control group, AGEs group. MTT assay was used to measure cell viability. Necrosis was determined by LDH release, and apoptosis was detected through TUNEL assay. ERS-related proteins were surveyed by western blot.
Results Compared with the control group, AGEs (200, 400, 600 μg/ml) resulted in a decrease of cell viability and an increase of LDH release, which was time (48, 72 h) and concentration dependent. Moreover, AGEs upregulated ERS-related proteins, including GRP 78, CHOP, leading to cardiomyocyte apoptosis.
Conclusions These findings demonstrate that AGEs induces cardiomyocyte apoptosis, and upregulates ERS-related protein levels including GRP 78 and CHOP. It demonstrates that endoplasmic reticulum stress plays an important role in the process of AGEs-induced cardiomyocyte apoptosis.