The class III
histone deacetylase sirtuin 1 (
SIRT1) plays a pivotal role in numerous biological and physiological functions, including
inflammation. An association between
SIRT1 and proinflammatory
cytokines might exist. In addition to their important role in
inflammation associated with
rheumatoid arthritis (RA), proinflammatory
cytokines mediate the development of systemic effects. Here, we evaluated systemic
SIRT1 expression and enzymatic activity, in peripheral blood mononuclear cells (PBMCs) and in liver isolated from rats with adjuvant-induced
arthritis (AIA), treated or not with low or high doses of
glucocorticoids (GCs). We also measured the production of tumour
necrosis factor alpha (TNF) and
interleukin-1 beta (IL-1 beta) in PBMCs and liver. We found that
SIRT1 expression and activity increased in PBMCs of AIA rats compared to healthy controls and decreased under GC treatment. Similarly, we observed an increased
SIRT1 activity in the liver of AIA rats compared to healthy controls which decreased under high doses of GCs. We also found an increase in
IL-1 beta and TNF levels in the liver of AIA rats compared to healthy controls, which decreased under high doses of GC. We did not observe a significant correlation between
SIRT1 activity and proinflammatory
cytokine production in PBMC or liver. In contrast, a strong positive correlation was found between the liver levels of TNF and
IL-1 beta (rho=0.9503, p=7.5x10-21). Our results indicate that increased
inflammation in AIA rats compared to healthy control is accompanied by an increased
SIRT1 activity in both PBMCs and liver, which could be decreased under GC treatment.