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Chinese Journal of Clinical Pharmacology and Therapeutics ›› 2011, Vol. 16 ›› Issue (6): 611-616.

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Effect and mechanism of radix astragali injection on production of inflammatory factors induced by lipopolysaccharide in human umbilical vein endothelial cells

LIANG Rong-shou, LI Jian-zhe   

  1. Department of Pharmacy, Ruikang Hospital, Guangxi College of Traditional Chinese Medicine, Nanning 530011, Guangxi, China
  • Received:2010-12-23 Revised:2011-05-26 Published:2011-07-25

Abstract: AIM: To observe the effect of radix astragali injection on the production of inflammatory factors induced by lipopolysaccharide (LPS) and investigate the anti-inflammation mechanism of radix astragali injection. METHODS: The human umbilical vein endothelial cells (HUVECs) were treated with LPS (1 mg/L) for 24 h following pretreatment with various concentrations of radix astragali injection (10, 20 or 40 mg/L) for 2 h. Cell viability was detected by MTT; The mRNA expression and levels of intercellular adhesion molecule-1 (ICAM-1), interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α) were determinded by reverse transcription-polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) respectively; The mRNA expression of Toll-like receptor 4 (TLR4) was measured by real-time quantitative reverse transcription-polymerase chain reaction (real-time RT-PCR) and the activity of nuclear factor kappa B (NF-κB) was assayed by electrotracellular mobility shift assay (EMSA). RESULTS: LPS could significantly decrease the cell viability, increase the mRNA expression and levels of ICAM-1, IL-8 and TNF-α, upregulate the expression of TLR4 mRNA and NF-κB acitivity. However, the aboving effects of LPS were markedly inhibited by pretreatment with radix astragali injection. CONCLUSION: Radix astragali injection inhibits the production of inflammatory factors may be associated with depressing the TLR4/ NF-κB signaling pathway.

Key words: Radix astragali injection, Lipopolysaccharide, Endothelial cell, Toll-like receptors 4, Nuclear factor-κB, Inflammatory factor

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