title: n-Butanol extracts of Panax notoginseng suppress LPS-induced MMP-2 expression in periodontal ligament fibroblasts and inhibit osteoclastogenesis by suppressing MAPK in LPS-activated RAW264.7 cells.
abstract: OBJECTIVE
  Periodontitis is a group of inflammatory diseases that affect connective tissue attachments and the supporting bone that surround the teeth. Osteoclasts are responsible for skeletal modeling and remodeling but may also destroy bone in several bone diseases, including osteoporosis and periodontitis. This study examined the anti-inflammatory effects of Panax notoginseng (PN) on periodontal ligament fibroblasts (PDLFs) and RAW264.7 cells under lipopolysaccharide (LPS) induced inflammatory conditions.
  
  
  METHODS
  The effects of PN on PDLFs were determined by measuring the cell viability and mRNA expression of tissue-destructive proteins. The effects of PN on osteoclasts were examined by measuring the following: (1) the cell viability, (2) the formation of Tartrate-resistant acid phosphatase (TRAP)(+) multinucleated cells, (3) MAPK signaling pathways, (4) mRNA expression of inflammatory-related proteins and (5) nitric oxide (NO) production.
  
  
  RESULTS
  The n-butanol extracts of PN (bPN) increased the cell proliferation of the PDLFs and decreased the mRNA expression of matrix metalloproteinase (MMP)-2 in the PDLFs. bPN inhibited the formation of LPS-stimulated TRAP(+) multinucleated cells. bPN also inhibited the LPS-stimulated activation of JNK and ERK signaling, and inhibited the LPS-stimulated degradation of I(K)B in the RAW264.7 cells. In addition, bPN decreased the mRNA expression of MMP-9 and iNOS, which are involved in the range of pathophysiological processes, such as inflammation in the RAW264.7 cells. NO production was also decreased via the inhibition of iNOS.
  
  
  CONCLUSIONS
  These findings suggest that bPN has therapeutic effects on bone-destructive processes, such as those that occur in periodontal diseases.
authors.affiliation: WCU Department of Nanobiomedical Sciences, Dankook University, Republic of Korea.
authors.forename: Young-Joo
authors.initials: YJ
authors.lastname: Jang
authors.forename: Mee-Eun
authors.initials: ME
authors.lastname: Kim
authors.forename: Seon-Yle
authors.initials: SY
authors.lastname: Ko
mesh_terms: D020001:1-Butanol / Q000494:pharmacology*; D002460:Cell Line; D002470:Cell Survival; D005347:Fibroblasts / Q000187:drug effects / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000188:drug therapy*; D018836:Inflammation Mediators / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology; D020935:MAP Kinase Signaling System / Q000187:drug effects; D008264:Macrophages / Q000187:drug effects / Q000378:metabolism; D020778:Matrix Metalloproteinase 2 / Q000096:biosynthesis*; D061965:Matrix Metalloproteinase Inhibitors; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors; D010010:Osteoclasts / Q000187:drug effects; D053723:Panax notoginseng; D010513:Periodontal Ligament / Q000166:cytology / Q000187:drug effects* / Q000201:enzymology; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology* / Q000627:therapeutic use*
chemical_list: D018836:Inflammation Mediators; D008070:Lipopolysaccharides; D061965:Matrix Metalloproteinase Inhibitors; D010936:Plant Extracts; D020001:1-Butanol; D052247:Nitric Oxide Synthase Type II; D020778:Matrix Metalloproteinase 2