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Ginsenoside Rb1 promotes angiogenesis potentially by activating the JAK-STAT3 signalling pathway

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Title Statement Ginsenoside Rb1 promotes angiogenesis potentially by activating the JAK-STAT3 signalling pathway
 
Added Entry - Uncontrolled Name Gong, zhi qiang; Guangxi University of Chinese Medicine Guangxi Minzu University
Han, Sha ; Guangxi University of Chinese Medicine
Liu, Xianfu ; Guangxi University of Chinese Medicine
Tang, Wenjun ; Guangxi University of Chinese Medicine
Meng, Tianxiu ; Guangxi University of Chinese Medicine
Huang, Yanhong
Yang, Lifang ; Guangxi Minzu University
Li, Chenlin ; Guangxi University of Chinese Medicine
Basic Ability Improvement Project for Young and Middle-aged Teachers in Guangxi Universities (2020KY59011), Research Project of Key Scientific Faculty of Chinese Medical Science Guangxi University of Chinese Medicine (2019ZD002).
 
Uncontrolled Index Term Hindlimb ischemia; Ischemic heart disease (IHD); Revascularization
 
Summary, etc. Conventional revascularization strategies for ischemic heart disease (IHD) are designed to prompt reperfusion of the coronary artery to the salvaged cardiomyocytes. However, these strategies may cause myocardial reperfusion injuries. Therefore, a safe and effective strategy needs to be developed to improve the conventional strategies. Here, we investigated the pro-angiogenic effect of Ginsenoside Rb1 (Rb1) to provide the experimental basis for angiogenesis-mediated drug therapy of IHD. Thus, Human umbilical vein endothelial cells (HUVECs) were treated with either a vehicle or Rb1 at 4, 8, 12 or 16 μM for 24 h. A model of hindlimb ischemia was established using C57BL/6J mice. In sham-operated mice, only the femoral artery was isolated without ligation whereas the other operations and supplementation control group were consistent. The mice in the supplementation group were injected with Rb1 (50 mg/kg body wt./day) for 7 days. The results indicated that Rb1 promotes cell proliferation, adhesion, migration and tube formation in the HUVECs in a dose-dependent manner. The ED50 of Rb1 to improve cell adhesion is 8 μM. In mice, Rb1 promoted angiogenesis after the ligation of the femoral artery and ameliorated the ischemic conditions. Intriguingly, more blood flow recovery was observed in the Rb1 supplemented mice than in the vehicle-treated mice (0.85 ± 0.05 vs. 0.71±0.10 on day 3; 0.94±0.10 vs. 0.75±0.08 on day 7). In HUVECs, Rb1 increased the phosphorylation of STAT3 and JAK, which may be the mechanism through which Rb1 mitigates IHD. Moreover, our results confirmed that Rb1mitigates IHD potentially by activating the JAK-STAT3 pathway. Further clinical trials are warranted to verify the clinical implications of Rb1.
 
Publication, Distribution, Etc. Indian Journal of Experimental Biology (IJEB)
2022-10-25 13:59:06
 
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http://op.niscair.res.in/index.php/IJEB/article/view/63414
 
Data Source Entry Indian Journal of Experimental Biology (IJEB); ##issue.vol## 60, ##issue.no## 11 (2022): IJEB [NOVEMBER 2022]
 
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