Open Access

Icariin reduces high glucose‑induced endothelial progenitor cell dysfunction via inhibiting the p38/CREB pathway and activating the Akt/eNOS/NO pathway

  • Authors:
    • Sisi Chen
    • Zhenya Wang
    • Heng Zhou
    • Bo He
    • Dan Hu
    • Hong Jiang
  • View Affiliations

  • Published online on: October 25, 2019     https://doi.org/10.3892/etm.2019.8132
  • Pages: 4774-4780
  • Copyright: © Chen et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

High glucose (HG) impairs endothelial progenitor cell (EPC) function. The activation of p38 mitogen‑activated protein kinase and the inhibition of the Akt/eNOS/NO pathway serve central roles in this process. Icariin has protective effects in endothelial cells. The aim of the present study was to investigate the effects of icariin on HG‑induced EPC dysfunction, including proliferation, migration and tube formation. Experiments were performed with EPCs isolated from the femurs and tibias of Sprague‑Dawley rats in vitro. In a dose‑dependent manner, icariin reversed the inhibition of EPC proliferation induced by HG treatment, and the maximal effective concentration of icariin was 1 µM [Fold change (FC):0.90±0.07, P=0.0124 vs. HG group]. The impaired EPC migration and tube formation induced by glucose was partially restored by 1 µM icariin treatment (FC: 0.81±0.08, P=0.0148 vs. HG group for migration; 0.82±0.03, P=0.0214 vs. HG group for tube formation). Furthermore, icariin significantly suppressed HG‑induced p38 and cAMP response element binding protein (CREB) phosphorylation in EPCs (FC: 1.84±0.21, P=0.0238 vs. HG group for p38; FC: 2.24±0.15, P=0.0068 vs. HG group for CREB). Increased Akt and endothelial nitric oxide (NO) synthase (eNOS) activation was also observed after icariin treatment (FC: 0.64±0.08, P=0.0047 vs. HG group for Akt; FC:0.53±0.05, P=0.0019 vs. HG group for eNOS), which was followed by increased NO production (FC: 0.69±0.06, P=0.0064 vs. HG group). In conclusion, icariin attenuated HG‑induced EPC dysfunction, which may be partially attributed to the inhibition of the p38/CREB pathway and the activation of the Akt/eNOS/NO pathway. Icariin may be a therapeutic candidate for improving the function of EPC.

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December 2019
Volume 18 Issue 6

Print ISSN: 1792-0981
Online ISSN:1792-1015

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Copy and paste a formatted citation
APA
Chen, S., Wang, Z., Zhou, H., He, B., Hu, D., & Jiang, H. (2019). Icariin reduces high glucose‑induced endothelial progenitor cell dysfunction via inhibiting the p38/CREB pathway and activating the Akt/eNOS/NO pathway. Experimental and Therapeutic Medicine, 18, 4774-4780. https://doi.org/10.3892/etm.2019.8132
MLA
Chen, S., Wang, Z., Zhou, H., He, B., Hu, D., Jiang, H."Icariin reduces high glucose‑induced endothelial progenitor cell dysfunction via inhibiting the p38/CREB pathway and activating the Akt/eNOS/NO pathway". Experimental and Therapeutic Medicine 18.6 (2019): 4774-4780.
Chicago
Chen, S., Wang, Z., Zhou, H., He, B., Hu, D., Jiang, H."Icariin reduces high glucose‑induced endothelial progenitor cell dysfunction via inhibiting the p38/CREB pathway and activating the Akt/eNOS/NO pathway". Experimental and Therapeutic Medicine 18, no. 6 (2019): 4774-4780. https://doi.org/10.3892/etm.2019.8132