Danhong injection mobilizes endothelial progenitor cells to repair vascular endothelium injury via upregulating the expression of Akt, eNOS and MMP-9

Hu, Zhen; Wang, Hong; 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/j.phymed.2019.152850

Cited by 36 publications

(23 citation statements)

References 23 publications

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“…SalD also showed potential antiplatelet activity and peroxidase inhibition effect [46,47]. And SalD has been identified as a valuable compound found in the Danhong injection used to relieve vascular endothelium impairment, which is used clinically for acute myocardial infarction [48]. SalD has also been screened as a potentially active component of the Shenxiong glucose injection, a pharmaceutical preparation for acute ischemic stroke in China [49].…”

Section: Introductionmentioning

confidence: 99%

Salvianolic Acid D Alleviates Cerebral Ischemia-Reperfusion Injury by Suppressing the Cytoplasmic Translocation and Release of HMGB1-Triggered NF-κB Activation to Inhibit Inflammatory Response

Zhang

Song

Wan

et al. 2020

Mediators of Inflammation

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Inflammatory response participates in the overall pathophysiological process of stroke. It is a promising strategy to develop antistroke drugs targeting inflammation. This study is aimed at investigating the therapeutic effect and anti-inflammatory mechanism of salvianolic acid D (SalD) against cerebral ischemia/reperfusion (I/R) injury. A rat middle cerebral artery occlusion/reperfusion (MCAO/R) injury model was established, and an oxygen-glucose deprivation/reoxygenation (OGD/R) injury model was established in PC12 cells. Neurological deficit score, cerebral infarction, and edema were studied in vivo. Cell viability was achieved using the MTT method in vitro. The Bax, Bcl-2, cytochrome c, HMGB1, TLR4, TRAF6, NF-κB p65, p-NF-κB p65, and cleaved caspase-3 and -9 were tested via the Western blot method. Cytokines and cytokine mRNA, including TNF-α, IL-1β, and IL-6, were studied via ELISA and PCR methods. The translocation of HMGB1 and NF-κB were studied by immunofluorescence assay. The HMGB1/NeuN, HMGB1/GFAP, and HMGB1/Iba1 double staining was carried out to observe the localization of HMGB1 in different cells. Results showed that SalD alleviated neurological impairment, decreased cerebral infarction, and reduced edema in I/R rats. SalD improved OGD/R-downregulated PC12 cell viability. SalD also promoted Bcl-2 expression and suppressed Bax, cytochrome c, and cleaved caspase-3 and -9 expression. SalD decreased the intensity of TLR4, MyD88, and TRAF6 proteins both in vivo and in vitro, and significantly inhibited the NF-κB nuclear translocation induced by I/R and OGD/R. What’s more, SalD inhibited HMGB1 cytoplasmic translocation in neurons, astrocytes, and microglia in both the cortex and hippocampus regions of I/R rats. In conclusion, SalD can alleviate I/R-induced cerebral injury in rats and increase the PC12 cell viability affected by OGD/R. The anti-inflammatory mechanism of SalD might result from the decreased nuclear-to-cytoplasmic translocation of HMGB1 and the inhibition on its downstream TLR4/MyD88/NF-κB signaling.

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Section: Introductionmentioning

confidence: 99%

Salvianolic Acid D Alleviates Cerebral Ischemia-Reperfusion Injury by Suppressing the Cytoplasmic Translocation and Release of HMGB1-Triggered NF-κB Activation to Inhibit Inflammatory Response

Zhang

Song

Wan

et al. 2020

Mediators of Inflammation

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“…Since the discovery of endothelial progenitor cells (EPCs) by Asahara et al in 1997 (1), it has been reported that EPCs are involved in vascular repair and postnatal angiogenesis (2). Following stimulation with various factors such as velvet antler, hydrogen sulfide and danhong, EPCs migrate to sites of injury to promote angiogenesis and repair vascular endothelial cell damage (3)(4)(5). The mechanism underlying EPC-mediated repair of injured endothelium is not only associated with differentiation and transdifferentiation into EPCs, but also with the biological functions of EPCs, including proliferation, migration and tube formation (6,7).…”

Section: Introductionmentioning

confidence: 99%

Role of the stromal cell derived factor‑1 in the biological functions of endothelial progenitor cells and its underlying mechanisms

et al. 2020

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Stromal cell derived factor-1 (SDF-1) is a chemokine that plays a critical role in the homing of stem and progenitor cells, including endothelial progenitor cells (EPCs). However, little research has been undertaken to evaluate the roles of SDF-1 in the biological functions of EPCs and related signaling pathways. The present study aimed to investigate the biological functions of EPCs in response to SDF-1, as well as the underlying mechanisms. The effects of SDF-1 treatment on EPC proliferation, migration and tube formation were assessed by performing MTS, Transwell and in vitro tube formation assays, respectively. The phosphorylation status of Akt and ERK was evaluated by western blotting. The present results indicated that SDF-1 treatment enhanced EPC proliferation, migration and tube formation compared with the control group. Furthermore, SDF-1-induced EPC proliferation was significantly reduced following treatment with a C-X-C Motif Chemokine Receptor 4 antagonist (AMD3100), a PI3K inhibitor (LY294002) and the mitogen-activated protein kinase kinase inhibitor (MEK; PD98059). SDF-1-induced migration and angiogenesis were significantly suppressed by the PI3K inhibitor, but not the MEK inhibitor. Moreover, SDF-1 significantly increased the protein expression levels of phosphorylated (p)-Akt and p-ERK; however, SDF-1-induced effects on protein expression were suppressed by AMD3100, LY294002 and PD98059. Thus, SDF-1-induced EPC proliferation was mediated by activation of the Akt and ERK signaling pathways, whereas SDF-1-mediated EPC migration and tube formation only involved activation of the Akt signaling pathway.

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“…Endothelial progenitor cells (EPCs) are precursor cells of vascular endothelial cells, which play an important role in the repair process of vascular endothelial injury (H. Hu et al, 2019; Z. Hu et al, 2019). The dysfunction of EPCs will destroy the dynamic balance between proliferation and apoptosis and further affect the repair process of damaged endothelial cells (Kong et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Functional damage of endothelial progenitor cells is attenuated by 14‐3‐3‐n through inhibition of mitochondrial injury and oxidative stress

Sun

Zhang

et al. 2020

Cell Biology International

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Endothelial progenitor cells (EPCs) are precursor cells of vascular endothelial cells, which are widely involved in the pathological process of cardiovascular diseases. EPCs apoptosis could accelerate the process of cardiovascular diseases. 14-3-3-η protein has been proved to be a potent antiapoptosis molecule. However, inhibition of EPCs apoptosis by 14-3-3-η and further specific mechanism have not been investigated. EPCs were isolated from human cord blood, and identified using VEGFR2 and CD34. 14-3-3-η overexpression model in vitro was established. Cell invasion, apoptosis, and proliferation were measured by transwell, flow cytometry, and Cell Counting Kit-8, respectively. Expression of 14-3-3-η, Bcl-2, and voltagedependent anion channel 1 (VDAC1) were measured using quantitative real-time polymerase chain reaction and western blot analysis. Reactive oxygen species (ROS) intensity was measured using 2ʹ-7ʹ dichlorofluorescin diacetate probe. Mitochondrial membrane potential was detected using JC-1 dye. Overexpression of 14-3-3-η significantly promoted invasion and proliferation, but suppressed apoptosis of EPCs. Overexpression of 14-3-3-η remarkably inhibited ROS and promoted antioxidant enzyme levels in EPCs. 14-3-3-η might inhibit apoptosis of EPCs through attenuating mitochondrial injury. This study might provide a new target, 14-3-3-η, for the prevention and treatment of cardiovascular diseases through targeting EPCs.

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Danhong injection mobilizes endothelial progenitor cells to repair vascular endothelium injury via upregulating the expression of Akt, eNOS and MMP-9

Cited by 36 publications

References 23 publications

Salvianolic Acid D Alleviates Cerebral Ischemia-Reperfusion Injury by Suppressing the Cytoplasmic Translocation and Release of HMGB1-Triggered NF-κB Activation to Inhibit Inflammatory Response

Salvianolic Acid D Alleviates Cerebral Ischemia-Reperfusion Injury by Suppressing the Cytoplasmic Translocation and Release of HMGB1-Triggered NF-κB Activation to Inhibit Inflammatory Response

Role of the stromal cell derived factor‑1 in the biological functions of endothelial progenitor cells and its underlying mechanisms

Functional damage of endothelial progenitor cells is attenuated by 14‐3‐3‐n through inhibition of mitochondrial injury and oxidative stress

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