Relaxin ameliorates high glucose-induced cardiomyocyte hypertrophy and apoptosis via the Notch1 pathway

Related Experiment Video

Updated: Feb 15, 2026

Derivation of Highly Purified Cardiomyocytes from Human Induced Pluripotent Stem Cells Using Small Molecule-modulated Differentiation and Subsequent Glucose Starvation
11:53

Derivation of Highly Purified Cardiomyocytes from Human Induced Pluripotent Stem Cells Using Small Molecule-modulated Differentiation and Subsequent Glucose Starvation

Published on: March 18, 2015

19.7K

Xiao Wei1, Yuan Yang1, Yin-Jiu Jiang2

  • 1Department of Cardiology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, P.R. China.

Experimental and Therapeutic Medicine
|February 6, 2018
PubMed

Insights

Relaxin (RLX) protects heart cells from high glucose damage by reducing apoptosis and hypertrophy. This protective effect is partly mediated by the Notch1 pathway and decreased oxidative stress.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Biology

Background:

  • High glucose (HG) can induce cardiomyocyte hypertrophy and apoptosis.
  • The molecular mechanisms underlying HG-induced cardiac cell damage are not fully understood.
  • Relaxin (RLX) may play a role in protecting cardiomyocytes.

Purpose of the Study:

  • To investigate the protective effects of RLX against HG-induced cardiomyocyte hypertrophy and apoptosis.
  • To elucidate the molecular mechanism of RLX's action, focusing on the Notch1 pathway and oxidative stress.

Main Methods:

  • H9c2 cells were treated with high glucose (33 mmol/l) with or without RLX (100 nmol/ml).
  • Assessed cell viability, apoptosis, oxidative stress markers (ROS, MDA, SOD), and hypertrophy markers (ANP, BNP).
  • Measured levels of Notch1, hes1, cytochrome C, and caspase-3; Notch inhibitor DAPT was used.

Main Results:

  • RLX increased H9c2 cell viability and reduced apoptosis in a time- and dose-dependent manner.
  • RLX suppressed reactive oxygen species and malondialdehyde, and enhanced SOD activity.
  • RLX partially reversed HG-induced changes in ANP, BNP, cytochrome C, caspase-3, Notch1, hes1, and MnSOD; DAPT abolished RLX's protective effects.

Conclusions:

  • RLX protects cardiomyocytes against high glucose-induced hypertrophy and apoptosis.
  • The protective effects of RLX are partly mediated through the Notch1 signaling pathway.
  • RLX may exert its cardioprotective effects by reducing oxidative stress.

Keywords:
apoptosisdiabetic cardiomyopathyhypertrophynotch pathwayoxidative stressrelaxin

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