Flower extract of Panax notoginseng attenuates lipopolysaccharide-induced inflammatory response via blocking of NF-kappaB signaling pathway in murine macrophages.
OBJECTIVE
The root of Panax notoginseng (PN) is commonly used to treat chronic liver disease with its therapeutic abilities to stop haemorrhage in the circulation, while the PN flower (PN-F) is largely unknown in the biological activities on inflammation and mechanisms of its actions. In this study, the pharmacologic effects of PN-F methanol extract on inflammation were investigated to address potential therapeutic or toxic effects in LPS-stimulated mouse macrophage cells, RAW264.7 cells.


METHODS
Production of NO, PGE2 and pro-inflammatory cytokines (TNF-alpha and IL-1beta) in supernatant, the expression of iNOS, COX-2 and cytokines, the phosphorylation of MAPK molecules (ERK1/2, JNK and p38 MAPK), and the activation of NF-kappaB in PN-F extract were assayed in LPS-stimulated RAW264.7 cells.


RESULTS
PN-F extract significantly inhibited the productions of NO, PGE2, TNF-alpha and IL-1beta on the LPS-stimulated RAW264.7 cells. In addition, PN-F extract suppressed the mRNA and protein expressions of iNOS, COX-2, TNF-alpha and IL-1beta in LPS-stimulated RAW264.7 cells. The molecular mechanism of PN-F extract-mediated attenuation in RAW264.7 cells has close a relationship to suppressing the phosphorylation of MAPK molecules such as ERK1/2, JNK and p38 MAPK, and the translocation of NF-kappaB p65 subunit into nuclear.


CONCLUSIONS
These results indicate that PN-F extract inhibits LPS-induced inflammatory response via the blocking of NF-kappaB signaling pathway in macrophages, and demonstrated that PN-F extract possesses anti-inflammatory properties in vitro.
Jung
Hyo-Won
HW
Department of Herbology, College of Oriental Medicine, Dongguk University, Gyeongju 780-714, South Korea.
Seo
Un-Kyo
UK
Kim
Jang-Hyun
JH
Leem
Kang-Hyun
KH
Park
Yong-Ki
YK
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D002460:Cell Line; D051546:Cyclooxygenase 2 / Q000378:metabolism; D015232:Dinoprostone / Q000037:antagonists & inhibitors; D048049:Extracellular Signal-Regulated MAP Kinases / Q000378:metabolism; D035264:Flowers; D051550:I-kappa B Kinase / Q000378:metabolism; D007249:Inflammation; D053583:Interleukin-1beta / Q000378:metabolism; D048031:JNK Mitogen-Activated Protein Kinases / Q000378:metabolism; D008070:Lipopolysaccharides; D008264:Macrophages; D051379:Mice; D016328:NF-kappa B / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors* / Q000378:metabolism; D053723:Panax notoginseng; D010936:Plant Extracts / Q000494:pharmacology*; D015398:Signal Transduction / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism
D000893:Anti-Inflammatory Agents; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D016328:NF-kappa B; D010936:Plant Extracts; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; D051550:I-kappa B Kinase; D048049:Extracellular Signal-Regulated MAP Kinases; D048031:JNK Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases; D015232:Dinoprostone