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The peroxisome proliferator-activated receptor (PPAR)-α activator, 5,8,11,14-eicosatetraynoic acid (ETYA), is an arachidonic acid analog. It is reported to inhibit up-regulation of pro-inflammatory genes. Among the inflammatory chemokines elaborated, glial cell-derived CCL2/MCP-1 is crucial, it promotes the migration and recruitment of inflammatory cells, it is primarily responsible for the initiation and progression of inflammatory responses in neurodegenerative disease and also associated with a variety of disease, including atherosclerosis.

ETYA has an anti-inflammatory mechanism, by increasing HuR-mediated-MKP-1 mRNA stability that leads to the specific suppression of CCL2/MCP-1 during inflammatory processes. Studies have shown that ETYA increases MKP-1 expression through HuR at the post-transcriptional level in a receptor-independent manner. Thereby providing evidence that ETYA is a potential therapeutic modulator of inflammation. ETYA's influence on suppressing CCL2/MCP-1 expression is an emerging therapeutic strategy for the treatment of neurodegenerative diseases such as Alzheimer's disease, multiple sclerosis, and brain ischemia.

A recent research regarding upper aerodigestive cancer ( an aggressive malignancy) has revealed that PPARγ pathways would be a novel therapy for this cancer. ETYA is a PPARγ activator and results from this study have shown that it down regulates cell proliferation and has antineoplastic features.

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