Chinese Journal of Tissue Engineering Research ›› 2011, Vol. 15 ›› Issue (37): 6956-6958.doi: 10.3969/j.issn.1673-8225.2011.37.027

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Hydroxysafflor yellow A promotes the proliferation of human umbilical vein endothelial cells

Sun Yu-qin1, 2, Han Hai-ling2, Song Wen-Gang2, Zhu Yu-Hong3, Lü Dong-Yan1, Zhu Yan-bin2, He Hai-tao2, Jiang Xin2   

  1. 1Department of Pathophysiology, School of Basic Medical Sciences, Jilin University, Changchun  130021, Jilin Province, China
    2Department of Cardiology and Brain, Affiliated Hospital of Beihua University, Jilin  132011, Jilin Province, China
    3Workers Hospital of Jilin Water Group Co.,Ltd., Jilin  132011, Jilin Province, China
  • Received:2011-03-06 Revised:2011-06-18 Online:2011-09-10 Published:2011-09-10
  • Contact: Sun Yu-qin, Associate professor, Master’s supervisor, Department of Pathophysiology, School of Basic Medical Sciences, Jilin University, Changchun 130021, Jilin Province, China; Department of Cardiology and Brain, Affiliated Hospital of Beihua University, Jilin 132011, Jilin Province, China 1206hhl@sina.com
  • About author:Sun Yu-qin, Associate professor, Master’s supervisor, Department of Pathophysiology, School of Basic Medical Sciences, Jilin University, Changchun 130021, Jilin Province, China; Department of Cardiology and Brain, Affiliated Hospital of Beihua University, Jilin 132011, Jilin Province, China 1206hhl@sina.com
  • Supported by:

    Major Technology R&D Program of Education Department of Jilin Province during 11th Five-Year Plan Period, No.2010123*

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Abstract:

BACKGROUND: The occurrence and development of cardiovascular diseases are related to the proliferation and apoptosis of vascular endothelial cells (VECs).
OBJECTIVE: To investigate the protective effects of hydroxysafflor yellow A (HSYA) on human VEC (hVEC) models.
METHODS: The hVECs cultured in vitro were interfered with HSYA and then were established into hVEC injury models by in vitro induction of lysophosphatidyl choline. A control group was set.
RESULTS AND CONCLUSION: Compared with the control group, hVECs proliferation was significantly decreased (P < 0.05), cell apoptosis was significantly increased (P < 0.05) and nitric oxide concentration was significantly decreased (P < 0.01) after lysophosphatidyl choline intervention. However, after treatment with HSYA, these symptoms could be reversed (P < 0.05). Results showed that HSYA could promote the proliferation of hVECs, inhibit cell apoptosis, and increase nitric oxide concentration, exhibiting protective effects on lysophosphatidyl choline-induced injury to hVECs.

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