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Journal of Chinese Pharmaceutical Sciences ›› 2015, Vol. 24 ›› Issue (1): 28-33.DOI: 10.5246/jcps.2015.01.003

• Original articles • Previous Articles     Next Articles

Vanadium regulates HSP60-induced IL-6 release from RAW264.7 cells in a dose-dependent manner

Wei Guo, Xiaoda Yang*   

  1. State Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University Health Science Center, Beijing 100191, China
  • Received:2014-08-28 Revised:2014-09-10 Online:2015-01-15 Published:2014-10-06
  • Contact: Tel.: 86-10-82801539, Fax: 86-10-62015584
  • Supported by:
    National Natural Science Foundation of China (Grant No. 21271012).

Abstract:

Vanadium compounds are promising anti-diabetic agents. However, the underlying mechanisms have not been fully elucidated. Inflammation and auto-immune disorders play important roles in the progresses of both type I and type II diabetes, in which heat shock protein 60 (HSP60) is an important endogenous inflammatory mediator. In the present work, we investigated the effects of vanadium compounds (vanadyl sulfate and sodium metavanadate) on the IL-6 production in RAW264.7 cells upon HSP60 stimulation. Our data revealed that both vanadyl ions regulated the IL-6 expression in a concentration-dependent manner. However, the two common NF-κB and PPAR-γ signal pathways were not involved in this process. Further works are needed to elucidate the underlying mechanism and significance of the immuno-modification actions for the pharmacological applications of anti-diabetic vanadium compounds.

Key words: Vanadyl ions, Heat shock protein 60, Interleukin-6

CLC Number: 

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