Evaluation of caspase-3 mRNA gene expression activity in amyloid beta-induced Alzheimer’s disease rats

Abstract

Caspase-3 plays a role in cell death in experimental models of several acute and chronic neurodegenerative disorders, caspase-3 activation has been proposed as an early neurodegenerative event in the progression of Alzheimer disease (AD). Alzheimer disease (AD) is a progressive neurodegenerative disease of the central nervous system characterized by neuropathological deposition of amyloid beta (Aβ) peptides, with the function as an extracellular signal molecule for caspase-3 activation in AD. Amyloid beta (Aβ) peptide is widely believed to play a central and etiological role in Alzheimer disease (AD). The overproduction of Aβ in the brain is a primary cause of AD and various research activities are conducted for inhibition of Aβ generation has become a hot topic in AD research. Therefore, in this study tried to make AD modeling through induction using Aβ, it is expected to increase the activity of caspase-3 mRNA which is the early sign of Alzheimer’s disease. Hence, the aim of this study was to evaluate caspase-3 mRNA levels in the wistar rat induced of Aβ. Twenty wistar rats were randomized into five groups K0: Without AD induction, K1: AD induction, K2: AD induction, K3: AD induction and K4: AD induction. Alzheimer’s disease (AD) induction was performed by Aβ1-42 (0.2 μg) injection at the intracerebroventricullary area. The mRNA Caspase-3 level measurements were performed by RT-PCR. The data caspase-3 mRNA gene expression was statistically analyzed by one-way ANOVA followed by Tukey’s test. Paired t-test analysis showed no significant differences of caspase-3 mRNA level before induction among 5 groups (p>0.05). At 6 weeks post-induction, there was significant increased caspase mRNA in all groups except K0 (p<0.05). Increased caspase-3 mRNA gene expression in amyloid beta-induced AD rats in all groups except K0 (p<0.05).