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Article

Tanshinone IIA inhibits high glucose‑induced proliferation, migration and vascularization of human retinal endothelial cells

  • Authors:
    • Keshun Fan
    • Suyan Li
    • Gaoqin Liu
    • Honghua Yuan
    • Li Ma
    • Peirong Lu
  • View Affiliations / Copyright

    Affiliations: Department of Ophthalmology, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China, Department of Ophthalmology, The First People's Hospital of Xuzhou, Xuzhou, Jiangsu 221002, P.R. China, Research Facility Center for Morphology of Xuzhou Medical University, Xuzhou, Jiangsu 221002, P.R. China
  • Pages: 9023-9028
    |
    Published online on: October 9, 2017
       https://doi.org/10.3892/mmr.2017.7743
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Abstract

Diabetic retinopathy is the most universal and severe complication of diabetes mellitus. The primary aim of the present study was to determine whether tanshinone IIA (TSA) has an inhibitory effect on the proliferation, migration and vascularization of human retinal endothelial cells (HREC) under high glucose (HG) conditions and the associated underlying mechanism. It was demonstrated that TSA exhibited a significant inhibitory effect on the proliferation, migration and vascularization of HRECs in a dose‑dependent manner, under conditions of high glucose (25 mM) medium. However, there was no distinct inhibitory effect on HREC proliferation, migration and vascularization under normal glucose (NG, 5.5 mM glucose) conditions. Reverse transcription‑quantitative polymerase chain reaction, western blotting and immunofluorescence experiments were conducted to evaluate the effects of TSA on the expression levels of vascular endothelial growth factor (VEGF) and intercellular adhesion molecule (ICAM)‑1. It was demonstrated that TSA significantly downregulated the expression levels of VEGF and ICAM‑1 in a dose‑dependent manner under HG conditions. Overall, the results of the present study indicate that TSA‑mediated inhibition of proliferation, migration and vascularization in HRECs may be associated with its ability to affect the expression levels of VEGF and ICAM‑1.
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Copy and paste a formatted citation
Spandidos Publications style
Fan K, Li S, Liu G, Yuan H, Ma L and Lu P: Tanshinone IIA inhibits high glucose‑induced proliferation, migration and vascularization of human retinal endothelial cells. Mol Med Rep 16: 9023-9028, 2017.
APA
Fan, K., Li, S., Liu, G., Yuan, H., Ma, L., & Lu, P. (2017). Tanshinone IIA inhibits high glucose‑induced proliferation, migration and vascularization of human retinal endothelial cells. Molecular Medicine Reports, 16, 9023-9028. https://doi.org/10.3892/mmr.2017.7743
MLA
Fan, K., Li, S., Liu, G., Yuan, H., Ma, L., Lu, P."Tanshinone IIA inhibits high glucose‑induced proliferation, migration and vascularization of human retinal endothelial cells". Molecular Medicine Reports 16.6 (2017): 9023-9028.
Chicago
Fan, K., Li, S., Liu, G., Yuan, H., Ma, L., Lu, P."Tanshinone IIA inhibits high glucose‑induced proliferation, migration and vascularization of human retinal endothelial cells". Molecular Medicine Reports 16, no. 6 (2017): 9023-9028. https://doi.org/10.3892/mmr.2017.7743
Copy and paste a formatted citation
x
Spandidos Publications style
Fan K, Li S, Liu G, Yuan H, Ma L and Lu P: Tanshinone IIA inhibits high glucose‑induced proliferation, migration and vascularization of human retinal endothelial cells. Mol Med Rep 16: 9023-9028, 2017.
APA
Fan, K., Li, S., Liu, G., Yuan, H., Ma, L., & Lu, P. (2017). Tanshinone IIA inhibits high glucose‑induced proliferation, migration and vascularization of human retinal endothelial cells. Molecular Medicine Reports, 16, 9023-9028. https://doi.org/10.3892/mmr.2017.7743
MLA
Fan, K., Li, S., Liu, G., Yuan, H., Ma, L., Lu, P."Tanshinone IIA inhibits high glucose‑induced proliferation, migration and vascularization of human retinal endothelial cells". Molecular Medicine Reports 16.6 (2017): 9023-9028.
Chicago
Fan, K., Li, S., Liu, G., Yuan, H., Ma, L., Lu, P."Tanshinone IIA inhibits high glucose‑induced proliferation, migration and vascularization of human retinal endothelial cells". Molecular Medicine Reports 16, no. 6 (2017): 9023-9028. https://doi.org/10.3892/mmr.2017.7743
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