Astragali Radix-Notoginseng Radix et Rhizoma medicine pair prevents cardiac remodeling by improving mitochondrial dynamic balance.
10.1016/S1875-5364(25)60806-5
- Author:
Pingping LIN
1
;
Hong CHEN
1
;
Zekun CUI
1
;
Boyang YU
1
;
Junping KOU
1
;
Fang LI
2
,
3
Author Information
1. Jiangsu Key Laboratory of TCM Evaluation and Translational Research, Research Center for Traceability and Standardization of TCMs, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 211198, China.
2. Jiangsu Key Laboratory of TCM Evaluation and Translational Research, Research Center for Traceability and Standardization of TCMs, School of Traditional Chinese Pharmacy, China Pharmaceutical University, Nanjing 211198, China. Electronic address: lifangcpu@
3. com.
- Publication Type:Journal Article
- Keywords:
Astragali Radix−Notoginseng Radix et Rhizoma medicine pair;
Cardiac fibrosis;
Cardiac hypertrophy;
Mitochondrial dynamics;
Transforming growth factor-β1/Smad3 pathway
- MeSH:
Animals;
Drugs, Chinese Herbal/pharmacology*;
Myocytes, Cardiac/metabolism*;
Mice;
Rats;
Male;
Mitochondrial Dynamics/drug effects*;
Ventricular Remodeling/drug effects*;
Astragalus Plant/chemistry*;
Mice, Inbred C57BL;
Rhizome/chemistry*;
Panax notoginseng/chemistry*;
Rats, Sprague-Dawley;
Natriuretic Peptide, Brain/genetics*;
Humans;
Angiotensin II;
Astragalus propinquus
- From:
Chinese Journal of Natural Medicines (English Ed.)
2025;23(1):54-63
- CountryChina
- Language:English
-
Abstract:
Astragali Radix (AR) and Notoginseng Radix et Rhizoma (NR) are frequently employed in cardiovascular disease treatment. However, the efficacy of the AR-NR medicine pair (AN) in improving cardiac remodeling and its underlying mechanism remains unclear. This study aimed to evaluate AN's cardioprotective effect and potential mechanism on cardiac remodeling using transverse aortic constriction (TAC) in mice and angiotensin II (Ang II)-induced neonatal rat cardiomyocytes (NRCMs) and fibroblasts in vitro. High-performance liquid chromatography-quadrupole-time of flight tandem mass spectrometry (HPLC-Q-TOF-MS/MS) characterized 23 main components of AN. AN significantly improved cardiac function in the TAC-induced mice. Furthermore, AN considerably reduced the serum levels of N-terminal pro-B-type natriuretic peptide (NT-proBNP), cardiac troponin T (CTn-T), and interleukin-6 (IL-6) and mitigated inflammatory cell infiltration. Post-AN treatment, TAC-induced heart size approached normal. AN decreased cardiomyocyte cross-sectional area and attenuated the upregulation of cardiac hypertrophy marker genes (ANP, BNP, and MYH7) in vivo and in vitro. Concurrently, AN alleviated collagen deposition in TAC-induced mice. AN also reduced the expression of fibrosis-related indicators (COL1A1 and COL3A1) and inhibited the activation of the transforming growth factor-β1 (TGF-β1)/mothers against decapentaplegic homolog 3 (Smad3) pathway. Thus, AN improved TAC-induced cardiac remodeling. Moreover, AN downregulated p-dynamin-related protein (Drp1) (Ser616) expression and upregulated mitogen 2 (MFN-2) and optic atrophy 1 (OPA1) expression in vivo and in vitro, thereby restoring mitochondrial fusion and fission balance. In conclusion, AN improves cardiac remodeling by regulating mitochondrial dynamic balance, providing experimental data for the rational application of Chinese medicine prescriptions with AN as the main component in clinical practice.
