İnvestigation of the potential protective effects of carvacrol on alzheimer's disease in in vitro and in vivo experimental models

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by impaired cognitive functions which appear as a result of loss of cortical and hippocampal neurons and synapses. Oxidative stress and hippocampal cholinergic loss caused by neuronal extracellular accumulation of amyloid-beta peptide (Aβ) are mostly held responsible for the pathogenesis of disease. In this study, we investigated therapeutic effects of carvacrol which has antioxidant and acetylcholinesterase inhibitor activities on AD at the cellular, tissue and systemic levels in-vitro neuron and in-vivo models of AD. Experimental AD models were established by adding Aβ to neuronal medium in-vitro groups and through bilateral intrahippocampal injection of Aβ to rats in-vivo groups. Cell viability, oxidant (malondialdehyde and hydrogen peroxide) and antioxidant (superoxide dismutase and catalase) parameters, Aβ1-40, Aβ1-42 and Tau peptide levels were measured by ELISA. Passive avoidance test was performed to in-vivo groups and the hippocampus was evaluated histopathologically. Data were compared by one-way ANOVA. Carvacrol decreased Aβ-induced oxidative stress parameters and increased antioxidant parameters and neuronal survival in vitro experiments. In in vivo experiments, carvacrol reduced Aβ-induced oxidative stress parameters and hippocampal neuronal damage, and also it shortened the time to pass into the dark compartment in the passive avoidance test. However, neither Aβ nor carvacrol changed plasma Aβ1-40, Aβ1-42 and Tau peptide, and hippocampal Tau peptide levels. Our findings demonstrated that carvacrol exhibits the ameliorating effects on Aβ-induced oxidative damage, hippocampal neuronal degeneration, and consequently the learning disruption in vitro, and in vivo AD models. Thus carvacrol may be a candidate to be choice in the treatment of AD.