Hippocampal neurons plated on poly L lysine coated glass coverslips and after-treatment with the indicated conditions, were immunostained using, anti PPARc, anti Tau 1 and anti p JNK antibodies. Neurons were analyzed using a Zeiss Pascal Confocal microscope, and morphometric analyses were completed using Image Pro plus application. we describe the JZL184 dissolve solubility effect of a few PPARc agonists in neurite and axonal elongation of hippocampal neurons. . We discovered that PPARc activation promotes axon elongation by a procedure that involved JNK activation. Therapy with TZDs somewhat increased axonal growth and using PPARc antagonists like GW 9662, removed axonal elongation caused by TZDs. Neurite outgrowth wasn’t notably improved by treatment with TZDs, suggesting that PPARc induced effects are especially strong on axonal growth. Pharmacological inhibitors of JNK process prevented TZDs induced axonal elongation, and more to the point, activation of PPARcsignificantly improved JNK activation on hippocampal neurons. Completely, these results suggest a novel position of PPARc taking part in axogenesis and neuronal polarity mediating activation of JNK. These observations confirm a possible use of PPARc activators from the neuronal injury seen in neurodegenerative diseases and extend previous studies that showed a protective role of PPARc in neurodegenerative diseases. Culture media, chemicals and serum were obtained from Sigma, Roche, locomotor system Merck, Gibco BRL and Calsein AM from Molecular Probes. . Troglitazone, rosiglitazone, ciglitazone, and GW 9662 were received from Cayman Chemical. The antibody anti tau 1 was kindly contributed by Dr. Alejandra Alvarez, antibodies, anti PPARc, anti whole JNK, anti p JNK, anti neurofilament, and anti p Extracellular transmission answer kinase antibodies were from Santa Cruz Biotechnology. 2Sprague Dawley rats found in these experiments were housed at the Faculty of Biological Sciences of the Pontificia Universidad natural product library Cato?lica de Chile and handled in accordance with recommendations specified and approved by the Institutional Animal Care and Use Committee at the Faculty of Biological Sciences of the Pontificia Universidad Cato?lica de Chile. 2Hippocampi from Sprague Dawley rats at embryonic day 18 were dissected, and primary hippocampal cultures were prepared as previously described. Pregnant dams were anesthetized with CO2 before obtaining the 18 day rat embryos used for that hippocampal cell cultures. All procedures were done in agreement with the animal handling and bioethical requirements established by Institutional Animal Care and Wellbeing Committee in the Faculty of Biological Sciences of the Pontificia Universidad Cato?lica de Chile. Hippocampal neurons were seeded in poly M lysine coated wells. Then, cultured hippocampal neurons were treated with RGZ, TGZ, PPARc agonists, and CGZ for 24, 48, and 72 h. During treatment, hippocampal neurons were observed and images were taken using video microscopy.