Curcumin ameliorates autoimmune diabetes. Evidence in accelerated murine models of type 1 diabetes

Proinflammatory cytokine NOD mice Adoptive Cell Transfer
DOI: 10.1111/cei.12322 Publication Date: 2014-03-13T14:03:57Z
ABSTRACT
Summary Type 1 diabetes (T1DM) is a T cell-mediated autoimmune disease that selectively destroys pancreatic β cells. The only possible cure for T1DM to control autoimmunity against cell-specific antigens. We explored whether the natural compound curcumin, with anti-oxidant and anti-inflammatory activities, might down-regulate cell response cells improve outcome in diabetes. employed two accelerated models: (i) cyclophosphamide (CYP) administration non-obese diabetic (NOD) mice (ii) adoptive transfer of diabetogenic splenocytes into NODscid mice. Curcumin treatment led significant delay onset, some instances prevented by inhibiting leucocyte infiltration preserving insulin-expressing To investigate mechanisms protection we studied effect curcumin on key immune populations involved pathogenesis disease. modulates lymphocyte impairing proliferation interferon (IFN)-γ production through modulation T-box expressed (T-bet), transcription factor proinflammatory helper type (Th1) differentiation, both at transcriptional translational levels. Also, reduces nuclear (NF)-κB activation receptor (TCR)-stimulated NOD lymphocytes. In addition, impairs stimulatory function dendritic reduced secretion cytokines nitric oxide (NO) low surface expression co-stimulatory molecules, leading an overall diminished antigen-presenting activity. These in-vitro effects correlated ex-vivo analysis obtained from curcumin-treated during course findings reveal effective therapeutic its actions responsible death.
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