PPAR Research / 2008 / Article / Tab 2 / Review Article
PPAR-
𝛾
, Microglial Cells, and Ocular Inflammation: New Venues for Potential Therapeutic Approaches Table 2 PPAR agonists and EAE.
Agonists Biological activity Receptor References Troglitazone Amelioration
of clinical symptoms. Reduced expression of proinflammatory
cytokines, IL1β
and TNF-α PPAR-
[129 ] Ciglitazone, 15d-PGJ2 Decrease
of severity and duration of clinical
paralysis. Decrease of CNS inflammation and
demyelination. Decrease of IL-12 production PPAR-
[130 ] 15d-PGJ2 Delay
in the onset and decrease in the severity of disease.
Reduction of Con A- and MBP Ac1–11-reactive,
IFN-α - and IL-4-secreting cells PPAR-
[131 ] Pioglitazone Decreased
mRNA levels of iNOS and the chemokines MIP1 and RANTES in the central nervous
system PPAR-
[132 ] Gemfibrozil and fenofibrate Dose-dependent
suppression of lymphocyte proliferation. Promotion of IL-4 production and inhibition of IFN-γ production PPAR-
[133 ] GW0742 Improvement
of clinical recovery. Reduction of glial activation PPAR-
[134 ] Ciglitazone, 15d-PGJ2 Amelioration
of clinical and pathological symptoms. Inhibition of neural antigen-specific T cell proliferation PPAR-
[135 ] Gemfibroil Reduction
of incidence and clinical signs. Inhibition of the infiltration of
inflammatory cells into the CNS. Reduced expression of proinflammatory molecules such as iNOS, IL-1, IL-6, and TNF-α no PPAR-
[136 ] Pioglitazone Prevention
of relapse episodes and reduction of mean clinical scores during the
treatment period. Decrease of IFN-γ levels PPAR-
[137 ]
