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.

AgonistsBiological activityReceptorReferences

TroglitazoneAmelioration of clinical symptoms. Reduced expression of proinflammatory cytokines, IL1β and TNF-αPPAR- [129]
Ciglitazone, 15d-PGJ2Decrease of severity and duration of clinical paralysis. Decrease of CNS inflammation and demyelination. Decrease of IL-12 productionPPAR- [130]
15d-PGJ2Delay 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 cellsPPAR- [131]
PioglitazoneDecreased mRNA levels of iNOS and the chemokines MIP1 and RANTES in the central nervous systemPPAR- [132]
Gemfibrozil and fenofibrateDose-dependent suppression of lymphocyte proliferation. Promotion of IL-4 production and inhibition of IFN-γ productionPPAR- [133]
GW0742Improvement of clinical recovery. Reduction of glial activationPPAR- [134]
Ciglitazone, 15d-PGJ2Amelioration of clinical and pathological symptoms. Inhibition of neural antigen-specific T cell proliferationPPAR- [135]
GemfibroilReduction 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-αno PPAR- [136]
PioglitazonePrevention of relapse episodes and reduction of mean clinical scores during the treatment period. Decrease of IFN-γ levelsPPAR- [137]

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