Salidroside and tyrosol from Rhodiola protect H9c2 cells from ischemia/reperfusion-induced apoptosis

Life Sci. 2012 Sep 4;91(5-6):151-8. doi: 10.1016/j.lfs.2012.06.026. Epub 2012 Jul 4.

Abstract

Aims: Heart disease is the leading cause of death worldwide. Ischemia-reperfusion injury can lead to apoptotic death of heart cells and subsequently heart failure. Rhodiola is an herbal medicine with two main bioactive compounds--salidroside (SAL) and tyrosol (TYR). This study aimed to investigate whether these two compounds can prevent ischemia/reperfusion-induced apoptosis in H9c2 cells.

Main methods: Assays for total phenolics assay and Oxygen Radical Absorbance Capacity showed high antioxidant capacity of SAL and TYR. H9c2 cells were subjected to simulated ischemia/reperfusion (IR) in the presence and absence of SAL and/or TYR, and nuclei condensation, caspase-3 activity, cytochrome c release and JNK phosphorylation were determined.

Key findings: In H9c2 cells, IR can lead to a 5-fold increase in p-JNK level. Apoptotic nuclei condensation, caspase-3 activity and cytochrome c release were markedly elevated, indicating the occurrence of apoptosis. SAL and TYR caused a dose-dependent inhibition of nuclear condensation. Furthermore, SAL and TYR, separately and in combination, significantly reduced caspase-3 activity, cytochrome c release and JNK activation. The anti-apoptotic effect of the combination was markedly higher than that of SAL or TYR alone.

Significance: The inhibition of the JNK signaling pathway is the key mechanism for the cytoprotective effect of SAL and TYR in IR-induced apoptosis.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antioxidants / administration & dosage
  • Antioxidants / isolation & purification
  • Antioxidants / pharmacology
  • Apoptosis / drug effects
  • Caspase 3 / metabolism
  • Cell Line
  • Cytochromes c / metabolism
  • Dose-Response Relationship, Drug
  • Drug Therapy, Combination
  • Glucosides / administration & dosage
  • Glucosides / isolation & purification
  • Glucosides / pharmacology*
  • JNK Mitogen-Activated Protein Kinases / metabolism
  • MAP Kinase Signaling System / drug effects
  • Myocardial Reperfusion Injury / drug therapy*
  • Myocardial Reperfusion Injury / physiopathology
  • Myocytes, Cardiac / drug effects*
  • Myocytes, Cardiac / pathology
  • Phenols / administration & dosage
  • Phenols / isolation & purification
  • Phenols / pharmacology*
  • Phenylethyl Alcohol / administration & dosage
  • Phenylethyl Alcohol / analogs & derivatives*
  • Phenylethyl Alcohol / isolation & purification
  • Phenylethyl Alcohol / pharmacology
  • Phosphorylation / drug effects
  • Rats
  • Rhodiola / chemistry*

Substances

  • Antioxidants
  • Glucosides
  • Phenols
  • 4-hydroxyphenylethanol
  • Cytochromes c
  • JNK Mitogen-Activated Protein Kinases
  • Caspase 3
  • rhodioloside
  • Phenylethyl Alcohol