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Uncovering the Molecular Mechanism of the Qiang-Xin 1 Formula on Sepsis-Induced Cardiac Dysfunction Based on Systems Pharmacology.
He, Shasha; Zhao, Jingxia; Xu, Xiaolong; Cui, Xuran; Wang, Ning; Han, Xuyang; Guo, Yuhong; Liu, Qingquan.
Afiliação
  • He S; Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, China.
  • Zhao J; Beijing Institute of Traditional Chinese Medicine, Beijing, China.
  • Xu X; Beijing Key Laboratory of Basic Research with Traditional Chinese Medicine on Infectious Diseases, Beijing, China.
  • Cui X; Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, China.
  • Wang N; Beijing Institute of Traditional Chinese Medicine, Beijing, China.
  • Han X; Beijing Key Laboratory of Basic Research with Traditional Chinese Medicine on Infectious Diseases, Beijing, China.
  • Guo Y; Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, China.
  • Liu Q; Beijing Institute of Traditional Chinese Medicine, Beijing, China.
Oxid Med Cell Longev ; 2020: 3815185, 2020.
Artigo em Inglês | MEDLINE | ID: mdl-32908632
ABSTRACT
Cardiac dysfunction is a critical manifestation of sepsis-induced multiorgan failure and results in the high mortality of sepsis. Our previous study demonstrated that a traditional Chinese medicine formula, Qiang-Xin 1 (QX1), ameliorates cardiac tissue damage in septic mice; however, the underlying pharmacology mechanism remains to be elucidated. The present study was aimed at clarifying the protective mechanism of the QX1 formula on sepsis-induced cardiac dysfunction. The moderate sepsis model of mice was established by cecal ligation and puncture surgery. Treatment with the QX1 formula improved the 7-day survival outcome, attenuated cardiac dysfunction, and ameliorated the disruption of myocardial structure in septic mice. Subsequent systems pharmacology analysis found that 63 bioactive compounds and the related 79 candidate target proteins were screened from the QX1 formula. The network analysis showed that the QX1 active components quercetin, formononetin, kaempferol, taxifolin, cryptotanshinone, and tanshinone IIA had a good binding activity with screened targets. The integrating pathway analysis indicated the calcium, PI3K/AKT, MAPK, and Toll-like receptor signaling pathways may be involved in the protective effect of the QX1 formula on sepsis-induced cardiac dysfunction. Further, experimental validation showed that the QX1 formula inhibited the activity of calcium/calmodulin-dependent protein kinase II (CaMKII), MAPK (P38, ERK1/2, and JNK), and TLR4/NF-κB signaling pathways but promoted the activation of the PI3K/AKT pathway. A cytokine array found that the QX1 formula attenuated sepsis-induced upregulated levels of serum IFN-γ, IL-1ß, IL-3, IL-6, IL-17, IL-4, IL-10, and TNF-α. Our data suggested that QX1 may represent a novel therapeutic strategy for sepsis by suppressing the activity of calcium, MAPK, and TLR4/NF-κB pathways, but promoting the activation of AKT, thus controlling cytokine storm and regulating immune balance. The present study demonstrated the multicomponent, multitarget, and multipathway characteristics of the QX1 formula and provided a novel understanding of the QX1 formula in the clinical application on cardiac dysfunction-related diseases.
Texto completo: Disponível Coleções: Bases de dados internacionais Base de dados: MEDLINE Tipo de estudo: Estudo prognóstico Idioma: Inglês Revista: Oxid Med Cell Longev Assunto da revista: Metabolismo Ano de publicação: 2020 Tipo de documento: Artigo País de afiliação: China

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Texto completo: Disponível Coleções: Bases de dados internacionais Base de dados: MEDLINE Tipo de estudo: Estudo prognóstico Idioma: Inglês Revista: Oxid Med Cell Longev Assunto da revista: Metabolismo Ano de publicação: 2020 Tipo de documento: Artigo País de afiliação: China