Due to the complex nature of Alzheimer's disease (AD), it is important to investigate agents with multiple effects in the treatment of AD. Carvacrol possesses anti-acetylcholinesterase, anti-oxidant, and neuroprotective properties. We therefore investigated therapeutic effects of carvacrol on cell viability, oxidative stress, and cognitive impairment in Aβ1-42-induced in vitro and in vivo models of AD. SH-SY5Y cells differentiated into neurons by retinoic acid were pretreated with carvacrol or galantamine before Aβ1-42 administration. For in vivo experiments, a rat model of AD was established by bilateral intrahippocampal injection of Aβ1-42. The groups received 1% DMSO, carvacrol, or galantamine intraperitoneally twice a day (morning and afternoon) for 6 days. Cell viability was determined using MTT and LDH tests. Learning and memory functions were assessed using a passive-avoidance test. Oxidant-antioxidant parameters (MDA, H₂ O₂ , SOD, and CAT) and Tau, Aβ1-40, and Aβ1-42 peptide levels in in vitro supernatant or in vivo serum and hippocampal samples were measured using ELISA. Carvacrol increased cell viability and exhibited a protective effect against oxidative stress by preventing Aβ1-42-induced cytotoxicity, LDH release, and increments in MDA and H₂ O₂ levels in vitro. Additionally, it improved memory impairment by reversing Aβ1-42-induced changes on passive-avoidance test. Carvacrol ameliorated Aβ1-42-induced increments in MDA and H₂ O₂ levels in in vitro supernatant and in vivo hippocampal samples. However, none of the treatments changed in vitro SOD and Tau-peptide levels, or in vivo serum levels of MDA, H₂ O₂ , SOD, CAT, Tau peptide, Aβ1-40, or Aβ1-42. Our results suggest that multi-target pharmacological agent carvacrol may be promising in treatment of AD by preventing beta-amyloid-induced neurotoxicity, oxidative stress, and memory deficits.

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