Armeniacae semen Extract Suppresses Lipopolysaccharide-Induced Expressions of Cycloosygenase-2 and Inducible Nitric Oxide Synthase in Mouse BV2 Microglial Cells

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  • Chang Hyun-Kyung
    Department of Physiology, College of Medicine, Kyung Hee University
  • Yang Hye-Young
    Department of Physiology, College of Medicine, Kyung Hee University
  • Lee Taeck-Hyun
    Department of Physiology, College of Medicine, Kyung Hee University
  • Shin Min-Chul
    Department of Physiology, College of Medicine, Kyung Hee University
  • Lee Myoung-Hwa
    Department of Physiology, College of Medicine, Kyung Hee University
  • Shin Mal-Soon
    Department of Physiology, College of Medicine, Kyung Hee University
  • Kim Chang-Ju
    Department of Physiology, College of Medicine, Kyung Hee University
  • Kim Ok-Jin
    Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee University
  • Hong Seon-Pyo
    Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee University
  • Cho Sonhae
    Department of Oriental Pharmaceutical Science, College of Pharmacy, Kyung Hee University

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Armeniacae semen is the seed of Prunus armeniaca L. var. ansu MAXIM which is classified into Rosaceae. In traditional oriental medicine, Armeniacae semen has been used for the treatment of pain and inflammatory diseases. In this study, the effect of Armeniacae semen extract on lipopolysaccharide-induced inflammation was investigated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, reverse transcription-polymerase chain reaction (RT-PCR), Western blot, prostaglandin E2 immunoassay, and nitric oxide detection on mouse BV2 microglial cells. In the present results, Armeniacae semen extract suppressed prostaglandin E2 synthesis and nitric oxide production by inhibiting the lipopolysaccharide-stimulated enhancement of cyclooxygenase-2 and inducible nitric oxide synthase mRNA expression in BV2 cells. These results show that Armeniacae semen exerts anti-inflammatory and analgesic effects probably by suppression of cyclooxygenase-2 and inducible nitric oxide synthase expressions.

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