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Chrysophanol protects against doxorubicin-induced cardiotoxicity by suppressing cellular PARylation

Jing Lu1, Jingyan Li1, Yuehuai Hu1

  • 1School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.

Acta Pharmaceutica Sinica. B
|August 7, 2019
PubMed

Keywords:
3AB, 3-aminobenzamideADR, adriamycinANOVA, one-way analysis of varianceApoptosisCHR, chrysophanolCMC-Na, sodium carboxymethylCO, cardiac outputCardiotoxicityChrysophanolCyt c, Cytochrome cDOX, doxorubicinDoxorubicinEF, ejection fractionFBS, fetal bovine serumFS, fractional shorteningHE, hematoxylin-eosinHR, heart rateIVSd, end-diastolic interventricular septumIVSs, end-systolic interventricular septumLV, end-systolic volumeLVEDV, LV end-diastolic volumeLVIDd, LV end-diastolic internal diameterLVIDs, LV end-systolic internal diameterLVPWd, LV end-diastolic posterior wall thicknessLVPWs, LV end-systolic posterior wall thicknessMitochondriaNS, normal salinePAR, polymers of ADP-ribosePARP1, poly(ADP-ribose) polymerase 1PARylated, poly(ADP-ribosyl)atedPARylationPARylation, poly(ADP-ribosyl)ationPBS, phosphate-buffered salineRCR, respiratory control ratioROS, reactive oxygen speciesRh123, rhodamine 123SD, Sprague–DawleyTUNEL, TdT-mediated dUTP nick end labelingVDAC1, voltage dependent anion channel 1

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