The assessment of vital responses of human and rat neuronal cells against to amyloid beta peptide and neuroactive steroid treatment [Amiloid beta peptit ve nöroaktif steroid uygulamasi{dotless}na karşi{dotless} i̇nsan ve si{dotless}çan nöronal hücrelerinin vital yani{dotless}tlari{dotless}ni{dotless}n deǧerlendirilmesi]

Amyloid beta (aβ) induced toxicity is an invitro neural degeneration model for alzheimer's disease. pregnenolone (p),pregnenolone sulphate (ps) are the major steroids produced in the neural tissue and are also called neuroactive steroids because of their behaviors like neurotransmitter. the synthesis of steroids in neural tissue could be changed by ischemia,oxidative stress or neurotoxicity namely induced by aβ,glutamate. the potential roles of p and ps in vital neuronal functions and in aβ peptide toxicity are not clearly identified. this work aims to investigate the effects of p,ps and aβ on the cell viability using two separate cell lines. the effects of conformational changes in aβ were also evaluated. rat pheochromocytoma (pc-12) and human neuroblastoma (shsy-5y) cell lines were treated with aβ25-35 (20/40μm) and variable concentrations of p and ps ranging from 0.25μm to 100μm. the cell viability was evaluated with mtt reduction assay and reverse-phase microscopy. the conformational changes of aβ peptides were induced with 72 hours incubation at 37°c. the structural changes of aβ were evaluated with electron microscopy. the treatment with 20μm aβ25-35 monomers did not affect shsy-5y cell viability,the significant toxicity was observed only with 40μm aβ 25-35 fibrils after 72hours. however the significant reduction in pc-12cell viability was obtained by the treatment with 20μm aβ 25-35 monomers. in pc-12 cell lines,the viability was decreased tõ40% of control group by the treatment with 1μm and higher concentrations of p and ps separately. this same effect was observed in shsy-5y cells with 5μm and higher concentrations of steroids.0.5μm p showed protective effect against aβ25-35 induced toxicity in both cell lines. our results suggest that aβ fibrillogenesis and neuroactive steroid may play causal roles in the neurodegenerative processes.