Isorhapontigenin protects against doxorubicin-induced cardiotoxicity
10.1016/j.apsb.2020.10.017
- Author:
Panxia WANG
1
;
Minghui WANG
1
;
Yuehuai HU
1
;
Jianxing CHEN
1
;
Yanjun CAO
1
;
Cui LIU
1
;
Zhongkai WU
2
;
Juan SHEN
3
;
Jing LU
1
;
Peiqing LIU
1
Author Information
1. School of Pharmaceutical Sciences, Sun Yat-sen University, Guangzhou 510006, China.
2. Department of Cardiac Surgery, First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, China.
3. Guangdong Provincial Key Laboratory of Pharmaceutical Bioactive Substances, Guangdong Pharmaceutical University, Guangzhou 510006, China.
- Publication Type:Journal Article
- Keywords:
AMPK, AMP-activated protein kinase;
AP-1, anti-microbial protein;
AREG, amphiregulin;
AUC/Dose, dose-normalized plasma exposures;
Amphiregulin;
Ang II, angiotensin II;
CO, cardiac output;
CTGF, connective tissue growth factor;
Cardiomyocytes apoptosis;
Cardiotoxicity;
Cmax/Dose, dose-normalized maximal plasma concentrations;
Connective tissue growth factor;
DAB, 3,3′-diaminobenzidine;
DMEM, Dulbecco's modified Eagle's medium;
Dob, dobutamine;
Dox, doxorubicin;
Doxorubicin;
EMT, epithelial mesenchymal transformation;
FOXO1, forkhead box class O1;
FS, fractional shortening;
HE, hematoxylin–eosin;
ISO, isoproterenol;
Isor, isorhapontigenin;
Isorhapontigenin;
LVAW;
d, left ventricular end-diastolic anterior wall thickness;
LVAW;
s, left ventricular end-systolic anterior wall thickness;
LVEF, left ventricular ejection fraction;
LVID;
d, left ventricular end-diastolic internal diameter;
LVID;
s, left ventricular end-systolic internal diameter;
LVPW;
d, left ventricular end-diastolic posterior wall thickness;
LVPW;
s, left ventricular end-systolic posterior wall thickness;
MAPK, mitogen-activated protein kinase;
MI, myocardial infarction;
NF-κB, nuclear factor kappa-B;
NRCMs, neonatal rat cardiomyocytes;
P2Y12 receptor, ADP receptor;
PGC-1α, peroxisome proliferator-activated receptor γ coactivator-1α;
PMSF, phenylmethanesulfonyl fluoride;
PVDF, polyvinylidene fluoride;
ROS, reactive oxygen species;
SD, Sprague–Dawley;
SDS-PAGE, sodium dodecyl sulfate-polyacrylamide gel electrophoresis;
SESN2, sestrin2;
TCF4, T-cell factor 4;
TEAD, TEA domain transcription factor proteins;
TEAD1;
TUNEL, TdT-mediated dUTP nick end labeling;
WGA, wheat germ agglutinin;
YAP1;
YAP1, Yes-associated protein 1;
qRT-PCR, quantitative real-time polymerase chain reaction;
sgRNAs, sequence guiding RNAs;
Δψm, mitochondrial membrane potential
- From:
Acta Pharmaceutica Sinica B
2021;11(3):680-693
- CountryChina
- Language:English
-
Abstract:
As an effective anticancer drug, the clinical limitation of doxorubicin (Dox) is the time- and dose-dependent cardiotoxicity. Yes-associated protein 1 (YAP1) interacts with transcription factor TEA domain 1 (TEAD1) and plays an important role in cell proliferation and survival. However, the role of YAP1 in Dox-induced cardiomyopathy has not been reported. In this study, the expression of YAP1 was reduced in clinical human failing hearts with dilated cardiomyopathy and Dox-induced
