PMID- 22487852
OWN - NLM
STAT- MEDLINE
DCOM- 20121213
LR  - 20220330
IS  - 1420-908X (Electronic)
IS  - 1023-3830 (Linking)
VI  - 61
IP  - 8
DP  - 2012 Aug
TI  - Anti-inflammatory effects of arbutin in lipopolysaccharide-stimulated BV2 
      microglial cells.
PG  - 817-25
LID - 10.1007/s00011-012-0474-2 [doi]
AB  - OBJECTIVES AND DESIGN: Arbutin, which is found in the genus Arctostaphylos, is an 
      anti-oxidant and a depigmenting agent. The present study was designed to validate 
      the anti-inflammatory effect of arbutin. MATERIALS AND METHODS: The 
      anti-inflammatory properties of arbutin were studied using a lipopolysaccharide 
      (LPS)-stimulated murine BV2 microglial cells model. As inflammatory parameters, 
      the production of nitric oxide (NO), inducible NO synthase (iNOS), 
      cyclooxygenase-2 (COX-2), tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta 
      (IL-1beta), monocyte chemoattractant protein-1 (MCP-1), and interleukin-6 (IL-6) 
      were evaluated. We also examined the expression of ninjurin1 (Ninj1) and the 
      adhesion activity of BV2 cells. Finally, we analyzed the activation of the 
      nuclear factor-kappaB (NF-kappaB) signaling pathway. RESULTS: Arbutin suppressed 
      LPS-induced production of NO and expression of iNOS and COX-2 in a dose-dependent 
      manner without causing cellular toxicity. Arbutin also significantly reduced 
      generation of proinflammatory cytokines, including IL-1beta and TNF-alpha, and other 
      inflammation-related genes such as MCP-1 and IL-6. Additionally, arbutin 
      suppressed the adhesion activity of BV2 cells and the expression of an important 
      adhesion molecule, Ninj1, in LPS-stimulated murine BV2 cells. Furthermore, 
      arbutin inhibited nuclear translocation and the transcriptional activity of 
      NF-kappaB. CONCLUSIONS: Taken together, our results suggest that arbutin might be 
      useful for treating the inflammatory and deleterious effects of BV2 microglial 
      cells activation in response to LPS stimulation.
FAU - Lee, Hyo-Jong
AU  - Lee HJ
AD  - College of Pharmacy, Inje University, Gimhae, Gyungnam, South Korea. 
      hjlee@inje.ac.kr
FAU - Kim, Kyu-Won
AU  - Kim KW
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120410
PL  - Switzerland
TA  - Inflamm Res
JT  - Inflammation research : official journal of the European Histamine Research 
      Society ... [et al.]
JID - 9508160
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Cell Adhesion Molecules, Neuronal)
RN  - 0 (Cytokines)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NF-kappa B)
RN  - 0 (Nerve Growth Factors)
RN  - 0 (Ninj1 protein, mouse)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - C5INA23HXF (Arbutin)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 1.14.13.39 (Nos2 protein, mouse)
RN  - EC 1.14.99.- (Ptgs2 protein, mouse)
RN  - EC 1.14.99.1 (Cyclooxygenase 2)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Arbutin/*pharmacology
MH  - Cell Adhesion/drug effects
MH  - Cell Adhesion Molecules, Neuronal/genetics
MH  - Cell Line
MH  - Cyclooxygenase 2/genetics
MH  - Cytokines/genetics
MH  - Lipopolysaccharides
MH  - Mice
MH  - Microglia
MH  - NF-kappa B/metabolism
MH  - Nerve Growth Factors/genetics
MH  - Nitric Oxide/metabolism
MH  - Nitric Oxide Synthase Type II/genetics
EDAT- 2012/04/11 06:00
MHDA- 2012/12/14 06:00
CRDT- 2012/04/11 06:00
PHST- 2011/12/02 00:00 [received]
PHST- 2012/03/23 00:00 [accepted]
PHST- 2012/03/19 00:00 [revised]
PHST- 2012/04/11 06:00 [entrez]
PHST- 2012/04/11 06:00 [pubmed]
PHST- 2012/12/14 06:00 [medline]
AID - 10.1007/s00011-012-0474-2 [doi]
PST - ppublish
SO  - Inflamm Res. 2012 Aug;61(8):817-25. doi: 10.1007/s00011-012-0474-2. Epub 2012 Apr 
      10.