Effect of danhong injection on the mobilisation of endothelial progenitor cells to vascular repair after percutaneous coronary intervention: a randomised controlled trial

Hu, Zhen; Hong, Wang; Fan, Guanwei; Zhang, Han; Wang, Xiaoying; Mao, Jingyuan; Zhao, Yingqiang; An, Yi; Huang, Yühong; Li, Chuan; Chang, Lianying; Chu, Xiangcheng; Li, Li; Li, Yanfen; Zhang, Yuan; Qin, Gangjian; Gao, Xiumei; Zhang, Boli

doi:10.1016/s0140-6736(16)31961-4

Cited by 7 publications

(5 citation statements)

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“…Our finding that endothelial inflammation as one of the most correlative mechanisms shared by DHI in the treatment of stroke and CAD is also supported by a number of observations from the bench to the bedside demonstrated that DHI exerted an anti-inflammatory effect 53 . In a recent clinical study, initial results from a randomized controlled trial suggested that DHI was effective in improving endothelial repair and protecting the endothelial lesion by mobilizing endothelial progenitor cells (EPCs) and inhibiting the inflammatory response after percutaneous coronary intervention in patients with CAD 52 . In patients with acute cerebral infarction, DHI was observed to lower the mRNA and protein levels of inflammatory cytokines (IL-6, TNF-α and IL-1β) and decreased nuclear NF-κB p65 expression in peripheral white blood cells 94 .…”

Section: Discussionmentioning

confidence: 99%

“…(2) Basic researches indicate that DHI can ameliorate cerebral ischemia-reperfusion injury 40 – 43 , cerebral ischemia damage 44 , myocardial reperfusion injury 45 , 46 , myocardial hypertrophy 47 , cardiac dysfunction 48 and cardiac ventricular remodeling 48 . (3) Pharmacological actions of DHI include antioxidation 49 , 50 , anticoagulation 51 , anti-inflammatory 52 – 54 , anti-fibrosis 55 , anti-angiogenesis 55 , anti-atherosclerosis 56 and anti-diabetes 57 effects. It is also capable of promoting vasodilation 58 , inhibiting vasoconstriction 59 and hyperlipidemia 60 .…”

Section: Introductionmentioning

confidence: 99%

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Network pharmacology exploration reveals endothelial inflammation as a common mechanism for stroke and coronary artery disease treatment of Danhong injection

Lyu

Yan

Liu

et al. 2017

Sci Rep

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Although Danhong injection (DHI) is the most widely prescribed Chinese medicine for both stroke and coronary artery disease (CAD), its underlying common molecular mechanisms remain unclear. An integrated network pharmacology and experimental verification approach was used to decipher common pharmacological mechanisms of DHI on stroke and CAD treatment. A compound-target-disease & function-pathway network was constructed and analyzed, indicating that 37 ingredients derived from DH (Salvia miltiorrhiza Bge., Flos Carthami tinctorii and DHI) modulated 68 common targets shared by stroke and CAD. In-depth network analysis results of the top diseases, functions, pathways and upstream regulators implied that a common underlying mechanism linking DHI’s role in stroke and CAD treatment was inflammatory response in the process of atherosclerosis. Experimentally, DHI exerted comprehensive anti-inflammatory effects on LPS, ox-LDL or cholesterol crystal-induced NF-κB, c-jun and p38 activation, as well as IL-1β, TNF-α, and IL-10 secretion in vascular endothelial cells. Ten of 14 predicted ingredients were verified to have significant anti-inflammatory activities on LPS-induced endothelial inflammation. DHI exerts pharmacological efficacies on both stroke and CAD through multi-ingredient, multi-target, multi-function and multi-pathway mode. Anti-endothelial inflammation therapy serves as a common underlying mechanism. This study provides a new understanding of DHI in clinical application on cardiovascular and cerebrovascular diseases.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Network pharmacology exploration reveals endothelial inflammation as a common mechanism for stroke and coronary artery disease treatment of Danhong injection

Lyu

Yan

Liu

et al. 2017

Sci Rep

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“…Tanshinone IIA may have the potential to protect EPCs against damage induced by tumor necrosis factor-α 103 . Danhong injection, extracted from Radix Salvia miltiorrhiza and Flos Carthamus tinctorius L, is effective in repairing endothelial lesions by mobilizing EPCs 104 .…”

Section: Epcs and Age-related Vascular Remodelingmentioning

confidence: 99%

Endothelial progenitor cells in age-related vascular remodeling

et al. 2018

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Accumulating evidence has demonstrated that endothelial progenitor cells (EPCs) could facilitate the reendothelialization of injured arteries by replacing the dysfunctional endothelial cells, thereby suppressing the formation of neointima. Meanwhile, other findings suggest that EPCs may be involved in the pathogenesis of age-related vascular remodeling. This review is presented to summarize the characteristics of EPCs and age-related vascular remodeling. In addition, the role of EPCs in age-related vascular remodeling and possible solutions for improving the therapeutic effects of EPCs in the treatment of age-related diseases are discussed.

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“…The destruction of integrity and activity of the endothelial layer is a key factor in the pathogenesis and progression of atherosclerosis [ 17 ]. Endothelial progenitor cells (EPCs) are a group of precursor cells that differentiate into mature endothelial cells [ 18 ]. Our study investigated the apoptosis-promoting effect of ADMA on EOCs, a sub-type of terminal EPCs, and then explored the underlining mechanism of the JNK pathway in endothelial regeneration.…”

Section: Discussionmentioning

confidence: 99%

Regulation of c-Jun N-Terminal Protein Kinase (JNK) Pathway in Apoptosis of Endothelial Outgrowth Cells Induced by Asymmetric Dimethylarginine

et al. 2017

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BackgroundEndothelial outgrowth cells (EOCs) are terminal endothelial progenitor cells (EPCs). Asymmetric dimethylarginine (ADMA) has been identified as a novel risk factor for cardiovascular diseases. Our aim in the present study was to investigate the effect of regulation of asymmetric dimethylarginine (ADMA) on EOCs apoptosis and to explore the underlining mechanisms of c-Jun N-terminal protein kinase (JNK) pathway in the process.Material/MethodsEOCs were harvested from umbilical cord blood and obtained by using density gradient centrifugation and adhesive culture methods. Endothelial characteristics were identified by immunohistochemistry and fluorescence staining. EOCs were treated with different concentrations of ADMA and detected by flow cytometry. After JNK specific inhibitor (SP600125) was added, EOCs apoptosis protein expressions were measured by Western blot analysis. Proliferation, migration, and vascularization were detected by CCK-8 assay, wound healing assay, and tube-like formation assay, respectively.ResultsEOCs were successfully extracted from umbilical cord blood and different concentrations of ADMA aggravated EOCs apoptosis. ADMA distinctly activates the phosphorylation activity of JNK. Supplementation of JNK-specific inhibitor (SP600125) decreased expression of Bax and cleaved caspase 3/9, and alleviated ADMA-induced apoptosis. SP600125 also promoted angiogenesis viability.ConclusionThe JNK pathway participates in the apoptosis-promoting process of EOCs, and targeted inhibition of the JNK pathway can alleviate ADMA-induced injury, which Is the potential underlying mechanism of vascular endothelium injury in ischemic stroke.

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Effect of danhong injection on the mobilisation of endothelial progenitor cells to vascular repair after percutaneous coronary intervention: a randomised controlled trial

Cited by 7 publications

References 0 publications

Network pharmacology exploration reveals endothelial inflammation as a common mechanism for stroke and coronary artery disease treatment of Danhong injection

Network pharmacology exploration reveals endothelial inflammation as a common mechanism for stroke and coronary artery disease treatment of Danhong injection

Endothelial progenitor cells in age-related vascular remodeling

Regulation of c-Jun N-Terminal Protein Kinase (JNK) Pathway in Apoptosis of Endothelial Outgrowth Cells Induced by Asymmetric Dimethylarginine

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