Article Text

PDF
GW24-e3090 Effects of EGB on AGEs-induced cardiomyocyte apoptosis: the involvement of endoplasmic reticulum stress
  1. Shen Mingzhi,
  2. Li Rongbin,
  3. Ou Shulin,
  4. Wang Chang,
  5. Mu Yang,
  6. Xu Yong
  1. Department of Cardiology, Hainan Branch of PLA General Hospital, Sanya, Hainan 572013, China

Abstract

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.

Statistics from Altmetric.com

Request permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.