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Exploring the Mechanism of Salvianolic Acid B against Myocardial Ischemia-Reperfusion Injury Based on Network Pharmacology.
Mao, Qianping; Shao, Chongyu; Zhou, Huifen; Yu, Li; Bao, Yida; Zhao, Yali; Yang, Jiehong; Wan, Haitong.
Afiliación
  • Mao Q; School of Life Sciences, Zhejiang Chinese Medicine University, Hangzhou 310053, China.
  • Shao C; School of Basic Medicine, Zhejiang Chinese Medicine University, Hangzhou 310053, China.
  • Zhou H; School of Basic Medicine, Zhejiang Chinese Medicine University, Hangzhou 310053, China.
  • Yu L; School of Basic Medicine, Zhejiang Chinese Medicine University, Hangzhou 310053, China.
  • Bao Y; School of Basic Medicine, Zhejiang Chinese Medicine University, Hangzhou 310053, China.
  • Zhao Y; School of Life Sciences, Zhejiang Chinese Medicine University, Hangzhou 310053, China.
  • Yang J; School of Basic Medicine, Zhejiang Chinese Medicine University, Hangzhou 310053, China.
  • Wan H; Research Institute of Traditional Chinese Medicine Encephalopathy, Zhejiang Chinese Medicine University, Hangzhou 310053, China.
Pharmaceuticals (Basel) ; 17(3)2024 Feb 28.
Article en En | MEDLINE | ID: mdl-38543095
ABSTRACT
This study aimed to explore the mechanisms through which salvianolic acid B (Sal-B) exerts its effects during myocardial ischemia-reperfusion injury (MI/RI), aiming to demonstrate the potential pharmacological characteristics of Sal-B in the management of coronary heart disease. First, Sal-B-related targets and MI/RI-related genes were compiled from public databases. Subsequent functional enrichment analyses using the protein-protein interaction (PPI) network, gene ontology (GO), and the Kyoto Encyclopedia of Genes and Genomes (KEGG) predicted the core targets and approaches by which Sal-B counters MI/RI. Second, a Sal-B-treated MI/RI mouse model and oxygen-glucose deprivation/reoxygenation (OGD/R) H9C2 cell model were selected to verify the main targets of the network pharmacological prediction. An intersectional analysis between Sal-B and MI/RI targets identified 69 common targets, with a PPI network analysis highlighting caspase-3, c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (p38) as central targets. GO and KEGG enrichment analyses indicated remarkable enrichment of the apoptosis pathway among these targets, suggesting their utility in experimental studies in vivo. Experimental results demonstrated that Sal-B treatment not only mitigated myocardial infarction size following MI/RI injury in mice but also modulated the expression of key apoptotic regulators, including Bcl-2-Associated X (Bax), caspase-3, JNK, and p38, alongside enhancing the B-cell lymphoma-2 (Bcl-2) expression, thereby inhibiting myocardial tissue apoptosis. This study leveraged an integrative network pharmacology approach to predict Sal-B's potential targets in MI/RI treatment and verified the involvement of key target proteins within the predicted signaling pathways through both in vivo and in vitro experiments, offering a comprehensive insight into Sal-B's pharmacological mechanism in MI/RI management.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Pharmaceuticals (Basel) Año: 2024 Tipo del documento: Article País de afiliación: China

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Idioma: En Revista: Pharmaceuticals (Basel) Año: 2024 Tipo del documento: Article País de afiliación: China
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