Suppressive effects of extracts from the aerial part of Coriandrum sativum L. on LPS-induced inflammatory responses in murine RAW 264.7 macrophages.
BACKGROUND
Coriandrum sativum is used not only as a spice to aid flavour and taste values in food, but also as a folk medicine in many countries. Since little is known about the anti-inflammatory ability of the aerial parts (stem and leaf) of C. sativum, the present study investigated the effect of aerial parts of C. sativum on lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophages. We further explored the molecular mechanism underlying these pharmacological properties of C. sativum.


RESULTS
Ethanolic extracts from both stem and leaf of C. sativum (CSEE) significantly decreased LPS-induced nitric oxide and prostaglandin E(2) production as well as inducible nitric oxide synthase, cyclooxygenase-2, and pro-interleukin-1beta expression. Moreover, LPS-induced IkappaB-alpha phosphorylation and nuclear p65 protein expression as well as nuclear factor-kappaB (NF-kappaB) nuclear protein-DNA binding affinity and reporter gene activity were dramatically inhibited by aerial parts of CSEE. Exogenous addition of CSEE stem and leaf significantly reduced LPS-induced expression of phosphorylated mitogen-activated protein kinases (MAPKs).


CONCLUSIONS
Our data demonstrated that aerial parts of CSEE have a strong anti-inflammatory property which inhibits pro-inflammatory mediator expression by suppressing NF-kappaB activation and MAPK signal transduction pathway in LPS-induced macrophages.
Wu
Trang-Tiau
TT
Department of Pediatric Surgery, Chung Shan Medical University Hospital, Taichung, Taiwan.
Tsai
Chia-Wen
CW
Yao
Hsien-Tsung
HT
Lii
Chong-Kuei
CK
Chen
Haw-Wen
HW
Wu
Yu-Ling
YL
Chen
Pei-Yin
PY
Liu
Kai-Li
KL
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000302:isolation & purification / Q000494:pharmacology / Q000627:therapeutic use*; D028526:Coriandrum / Q000737:chemistry; D017930:Genes, Reporter; D020672:I-kappa B Proteins / Q000378:metabolism; D007249:Inflammation / Q000139:chemically induced / Q000188:drug therapy* / Q000378:metabolism; D018836:Inflammation Mediators / Q000378:metabolism*; D008070:Lipopolysaccharides; D008264:Macrophages / Q000187:drug effects* / Q000378:metabolism; D051379:Mice; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism; D000072000:NF-KappaB Inhibitor alpha; D016328:NF-kappa B; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use*; D018515:Plant Leaves; D018547:Plant Stems; D015398:Signal Transduction / Q000187:drug effects*; D050863:Synaptotagmin I / Q000378:metabolism
D000893:Anti-Inflammatory Agents; D020672:I-kappa B Proteins; D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D016328:NF-kappa B; C000606205:Nfkbia protein, mouse; D010936:Plant Extracts; D050863:Synaptotagmin I; D000072000:NF-KappaB Inhibitor alpha; D020928:Mitogen-Activated Protein Kinases