PMID- 19407980
OWN - NLM
STAT- MEDLINE
DCOM- 20090514
LR  - 20131121
IS  - 0253-6269 (Print)
IS  - 0253-6269 (Linking)
VI  - 32
IP  - 4
DP  - 2009 Apr
TI  - Anti-inflammatory effect of Trichostatin-A on murine bone marrow-derived 
      macrophages.
PG  - 613-24
LID - 10.1007/s12272-009-1418-4 [doi]
AB  - Histone deacetylase (HDAC) inhibitors were recently shown to suppress 
      inflammatory responses in models of autoimmune and inflammatory diseases. In this 
      study, the anti-inflammatory effects of five different HDAC inhibitors on 
      lipopolysaccharide-(LPS)-stimulated macrophages were compared and the mechanisms 
      of these effects were demonstrated. Trichostatin-A (TSA) and scriptaid, two of 
      the five HDAC inhibitors, showed the most potent inhibitory effects on the 
      nitric-oxide (NO) production of RAW264.7 cells and bone-marrow-derived 
      macrophages (BMDMs). TSA significantly decreased the mRNA and protein levels of 
      the proinflammatory cytokines, such as tumor necrosis factor (TNF)-alpha, 
      interleukin (IL)-6, and IL-1beta, whereas the pretreatment with TSA increased the 
      level of the immunosuppressive cytokine IL-10. TSA also reduced the cell surface 
      markers of the maturity of the macrophages. Furthermore, a longer duration (up to 
      8 h) of hyperacetylation was observed in the cells that had been exposed to TSA, 
      whereas the hyperacetylation induced by the other HDAC inhibitors was absent 
      after 8 h. These results demonstrated that TSA is the most potent HDAC inhibitor 
      of histone deacetylation and has the greatest ability to induce anti-inflammatory 
      activity in cloned and naive macrophages. These results are expected to serve as 
      a guide for future studies on the ability of HDAC inhibitors to inhibit acute and 
      chronic inflammatory diseases.
FAU - Han, Sang-Bae
AU  - Han SB
AD  - College of Pharmacy, Chungbuk National University, Cheongju, 361-763, Korea.
FAU - Lee, Jae Kwon
AU  - Lee JK
LA  - eng
PT  - Comparative Study
PT  - Journal Article
DEP - 20090429
PL  - Korea (South)
TA  - Arch Pharm Res
JT  - Archives of pharmacal research
JID - 8000036
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Cytokines)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Histone Deacetylase Inhibitors)
RN  - 0 (Hydroxamic Acids)
RN  - 0 (Hydroxylamines)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Quinolines)
RN  - 0 (RNA, Messenger)
RN  - 0 (scriptaid)
RN  - 31C4KY9ESH (Nitric Oxide)
RN  - 3X2S926L3Z (trichostatin A)
RN  - EC 3.5.1.98 (Histone Deacetylases)
SB  - IM
MH  - Animals
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Cell Line
MH  - Cell Survival/drug effects
MH  - Cytokines/genetics/metabolism
MH  - Dose-Response Relationship, Drug
MH  - Enzyme Inhibitors/*pharmacology
MH  - *Histone Deacetylase Inhibitors
MH  - Histone Deacetylases/metabolism
MH  - Hydroxamic Acids/*pharmacology
MH  - Hydroxylamines/pharmacology
MH  - Inflammation Mediators/metabolism
MH  - Lipopolysaccharides/pharmacology
MH  - Macrophage Activation/drug effects
MH  - Macrophages/*drug effects/enzymology/immunology
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Nitric Oxide/metabolism
MH  - Quinolines/pharmacology
MH  - RNA, Messenger/metabolism
MH  - Time Factors
EDAT- 2009/05/02 09:00
MHDA- 2009/05/15 09:00
CRDT- 2009/05/02 09:00
PHST- 2009/01/23 00:00 [received]
PHST- 2009/03/26 00:00 [accepted]
PHST- 2009/03/26 00:00 [revised]
PHST- 2009/05/02 09:00 [entrez]
PHST- 2009/05/02 09:00 [pubmed]
PHST- 2009/05/15 09:00 [medline]
AID - 10.1007/s12272-009-1418-4 [doi]
PST - ppublish
SO  - Arch Pharm Res. 2009 Apr;32(4):613-24. doi: 10.1007/s12272-009-1418-4. Epub 2009 
      Apr 29.