Ginsenoside Rb1 promotes angiogenesis potentially by activating the JAK-STAT3 signalling pathway
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https://doi.org/10.56042/ijeb.v60i11.63414Title: Ginsenoside Rb1 promotes angiogenesis potentially by activating the JAK-STAT3 signalling pathwayAuthors:
Gong, ZhiqiangHan, ShaLiu, XianfuTang, WenjunMeng, TianxiuHuang, YanhongYang, LifangLi, ChenglinKeywords: Hindlimb ischemia;Ischemic heart disease (IHD);RevascularizationIssue Date: Nov-2022Publisher: NIScPR-CSIR, IndiaAbstract: 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.Page(s): 817-824ISSN: 0975-1009 (Online); 0019-5189 (Print)Appears in Collections:
IJEB Vol.60(11) [Nov 2022]Items in NOPR are protected by copyright, with all rights reserved, unless otherwise indicated.
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