
Therapeutic effects of Aconiti Lateralis Radix Praeparata combined with Zingiberis Rhizoma on doxorubicin‐induced chronic heart failure in rats based on an integrated approach
Author(s) -
Wen JianXia,
Li RuiSheng,
Wang Jian,
Hao JunJie,
Qin WeiHan,
Yang Tao,
Wang RuiLin,
Wei ShiZhang,
Liu XiaoYi,
Li HaoTian,
Wang JiaBo,
Liu HongHong,
Zhao YanLing
Publication year - 2020
Publication title -
journal of pharmacy and pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 118
eISSN - 2042-7158
pISSN - 0022-3573
DOI - 10.1111/jphp.13191
Subject(s) - pharmacology , heart failure , metabolomics , medicine , doxorubicin , therapeutic effect , cardiac function curve , biology , bioinformatics , chemotherapy
Objectives This study was aimed to explore the mechanism of Aconiti Lateralis Radix Praeparata (ALRP) and Zingiberis Rhizoma (ZR) on doxorubicin (DOX)‐induced chronic heart failure (CHF) in rats by integrated approaches. Methods Effects of ALRP and ZR on cardiac function, serum biochemical indicators and histopathology in rats were analysed. Moreover, UHPLC‐Q‐TOF/MS was performed to identify the potential metabolites affecting the pathological process of CHF. Metabolomics and network pharmacology analyses were conducted to illustrate the possible pathways and network in CHF treatment. The predicted gene expression levels in heart tissue were verified and assessed by RT‐PCR. Key findings ALRP‐ZR demonstrated remarkable promotion of hemodynamic indices and alleviated histological damage of heart tissue. Metabolomics analyses showed that the therapeutic effect of ALRP and ZR is mainly associated with the regulation of eight metabolites and ten pathways, which may be responsible for the therapeutic efficacy of ALRP‐ZR. Moreover, the results of RT‐PCR showed that ALRP‐ZR could substantially increase the expression level of energy metabolism‐related genes, including PPARδ , PPARγ , Lpl , Scd , Fasn and Pla2g2e . Conclusions The results highlighted the role of ALRP‐ZR in the treatment of CHF by influencing the metabolites related to energy metabolism pathway via metabolomics and network pharmacology analyses.