Role of licochalcone C in cardioprotection against ischemia/reperfusion injury of isolated rat heart via antioxidant, anti-inflammatory, and anti-apoptotic activities

Life Sci. 2015 Jul 1:132:27-33. doi: 10.1016/j.lfs.2015.04.008. Epub 2015 Apr 25.

Abstract

Aims: This study aimed to evaluate the protective effect of licochalcone C against myocardial ischemia/reperfusion injury in rats.

Main methods: Left ventricular developed pressure (LVDP) and its maximum up/down rate (±dp/dtmax) were recorded as myocardial function. Levels of creatine kinase (CK), lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), glutathione/glutathione disulfide (GSH/GSSG) ratio, and tumor necrosis factor-alpha (TNF-α) were determined by using enzyme-linked immunosorbent assay. Cell morphology was observed and mitochondrial damage was assessed by HE coloration and transmission electron microscopy, respectively. Cardiomyocyte apoptosis was determined by using terminal deoxynucleotidyl transferased UTP nick-end labeling (TUNEL).

Key findings: Pretreatment with licochalcone C significantly improved the recovery of LVDP and ±dp/dtmax, and increased the levels of SOD and GSH/GSSG ratio. However, pretreatment with licochalcone C not only decreased the TUNEL-positive cell ratio and morphological changes, but also weaken the mitochondrial injury and the levels of CK, LDH, MDA, and TNF-α.

Significance: These results suggested an important function of licochalcone C extracted from traditional Chinese medicine in the cardioprotection via antioxidant, anti-inflammatory, and anti-apoptotic activities.

Keywords: Anti-apoptotic; Anti-inflammatory; Antioxidant; Cardioprotection; Licochalcone C.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Animals
  • Anti-Inflammatory Agents / metabolism
  • Anti-Inflammatory Agents / pharmacology*
  • Antioxidants / metabolism
  • Antioxidants / pharmacology*
  • Apoptosis / drug effects*
  • Chalcones / metabolism
  • Chalcones / pharmacology*
  • Creatine Kinase / metabolism
  • Glutathione / metabolism
  • In Situ Nick-End Labeling
  • L-Lactate Dehydrogenase / metabolism
  • Malondialdehyde / metabolism
  • Rats
  • Reperfusion Injury / prevention & control*
  • Superoxide Dismutase / metabolism
  • Tumor Necrosis Factor-alpha / metabolism

Substances

  • Anti-Inflammatory Agents
  • Antioxidants
  • Chalcones
  • Tumor Necrosis Factor-alpha
  • Malondialdehyde
  • L-Lactate Dehydrogenase
  • Superoxide Dismutase
  • Creatine Kinase
  • Glutathione
  • licochalcone C