The use of cucurbitacin I in the inhibition of enzymes in the inflammatory mechanism that causes the accumulation of tau fibrils in an alzheimer animal model, and the investigation of its effect on memory acquisition by measuring the expression of the relevant genes

Alzheimer's disease (AD) is a progressive neurodegenerative disease. Phytochemicals have potential effective in the treatment of neurological diseases. Neurofibrils cause neuronal losses and contribution to the inflammation process in AD. In this thesis, the effect of cucurbitacin I (CuI) on hippocampal TAU accumulation, TDO2, and Nf-B genes expressions and gain of cognitive functions were investigated in an okadaic acid-induced AD rat model. 36 Sprague Dawley female rats (200-250 g) were divided into 6 groups (6 animals in each group). Groups; Control, artificial cerebrospinal fluid (aCSF), stereotaxic, stereotaxic+aCSF, stereotaxic+aCSF+CuI (2mg/kg), stereotaxic+aCSF+CuI (4mg/kg). Morris water maze (MWM) and the elevated plus maze test (EPM) were used for cognitive and anxiety analysis. Detection of hippocampal deposition of TAU fibrils was performed by immunohistochemical analysis. Expressions of two genes were analyzed by quantitative real-time PCR (qPCR) and protein expressions by western blotting. One-way ANOVA was used for statistical analyses. The results suggest that CuI may have therapeutic potential in the hippocampal reduction of TAU with the contribution of TDO2 and NF-B genes and acquisition of cognitive functions.