Protective effect of HDAC inhibitor for sepsis-associated acute lung injury

2014 Fiscal Year Final Research Report

• Project/Area Number: 24791586
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Anesthesiology/Resuscitation studies
• Research Institution: University of Toyama
• Principal Investigator: AOKI YUTA 富山大学, 大学病院, 助教 (10621667)
• Project Period (FY): 2012-04-01 – 2015-03-31
• Keywords: 敗血症 / ヒストン脱アセチル酵素 / 急性肺傷害

Outline of Final Research Achievements

Epigenetic regulation works through modifying the structures of DNA, making it more or less accessible to transcription. Histone acetylation is one of the types of epigenetic process. In this study, we examined whether histone deacetylase(HDAC) can contribute to sepsis-associated inflammation and apoptosis.
Treatment of novel broad-spectrum HDAC inhibitor suppressed apoptosis induction in lungs and spleens of septic mice. However, it failed to inhibit elevated levels of serum cytokines and prevent lung inflammation in septic mice. Valproic acid also showed antiapoptotic but not anti-inflammatory effects in septic mice.
The data with HDAC inhibitors suggest that imbalance in histone acetylation may play a contributory role in expression or repression of genes involved in septic cell apoptosis.

Free Research Field

敗血症