Research Projects

The omega 3 fatty acids (?3FAs) alleviate apoptosis in the neuro leading to a protection to the injured brain. However, their anti-apoptotic activity in astrocytes is obscure. IIcre, we hypothesized an an apoptotic role of w3FAs in the damaged developing astrocytes that may involve modulation in the levels of glial fibrillary acidic protein (GFAI peroxisome proliferator-activated receptors (PPAR), and the fatty acid binding 7 (FABP7), a strong binder of the w3I'As. The w3KAs we supplemented as a mixture of docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) to pregnant and lactating rats. The apoptosis in t rat astrocytes was then induced by a mixture of the metals, Pb, Cd and As (MM, metal mixture). The ?3FAs prevented the MM-induc attenuation in the GFAP levels, PPAR (alpha, delta and gamma and FABP7 in the brain tissues. The MM raised the levc of the PPARs in the GFAP-immunoreactive astrocytes, and omega 3 fatty acid prevented the increase. The MM up-regulated the lev« of FABP-7 in the astrocytes, and ?3 fatty acid maintained the up-regulated status, probably because of the binding of the fatty acids w: the FABP7. The MM promoted the translocation of PPAR alpha, delta and gamma to the nucleus and omega 3 fatty acid prevented. This, therefore, indicates that translocation of PPARs to nucleus damages astrocytes, and ?3 fatty acid prevents translocation and prevents astrocyte damage.