Objectives To investigate the effects of EGB on advanced glycosylation end products (AGEs)-induced cardiomyocyte injury, and the role of endoplasmic reticulum stress (ERS) in the process.
Methods Cultured neonatal rat cardiomyocytes were randomly divided into four groups: control, EGB, AGEs, and AGEs + EGB. 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 control group, AGEs (400 μg/ml) resulted in a decrease of cell viability and an increase of LDH release, which was time (48, 72 h) dependent. Moreover, AGEs upregulated ERS-related proteins, including GRP 78, CHOP, leading to cardiomyocyte apoptosis. EGB (50, 100 μg/ml) alone had no effect on cell viability, LDH release, apoptosis, and ERS-related proteins. Cotreatment of EGB and AGEs (400 μg/ml) alleviated AGEs-induced LDH release and apoptosis, improved cell viability, and downregulated ERS-related proteins including GRP 78 and CHOP. Overexpression of CHOP offset the protection of EGB on AGEs-induced injury in H9C2 cells.
Conclusions These findings demonstrate that EGB protects cardiomyocytes against AGEs-induced cardiomyocyte apoptosis. It may be associated with attenuation of endoplasmic reticulum stress.