Objective: With an eye toward its effects on striatal angiogenesis and the AMPK/ FOXO3 transcription factor O3 pathway, this work attempts to investigate the neuroprotective effect of Carvacrol in a mouse model of rotenone-induced Parkinson’s disease (PD).

Background: Using the inhibition of complex I and the activation of microglia features resulting in oxidative stress, inflammation, neurotoxicity, and changes in locomotor and behavioral activities, rotenone can generate a validated experimental model of Parkinson’s disease (PD). Research on diets heavy in antioxidants has shown that this may reduce the risk of neurodegenerative diseases. 

Method: Carvacrol 100 or 200 mg/kg/day over 18 days and rotarod and pole tests were used to evaluate mice given repeated doses of rotenone to generate Parkinson’s disease (PD) in the continuous study. The brains were removed and ready for immunohistochemical or biochemical testing. Among the angiogenic markers and oxidative stress indicators evaluated were malondialdehyde, reduced glutathione, hemoxygenase-1, vascular endothelial growth factor (VEGF the nuclear factor erythroid 2

Results: Carvacrol increased the motor ability of the mice, striatal glutathione, Nrf2, hemoxygenase-1, and thioredoxin. Carvacrol also raised the tyrosine hydroxylase (TH)-stained neurons found in the striatal neural terminals and in the substantia nigra neurons. Carvacrol also cleaved caspase 3 and downregulated VEGF. This study demonstrating AMPK- FOXO3 pathway activation and proangiogenic factor (VEGF) suppression as mediator of MTF’s neuroprotective action.

Conclusion: More study is needed to validate this procedure in next models of Parkinson’s disease and neurodegenerative diseases.

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MDS Abstracts - https://www.mdsabstracts.org/abstract/carvacrol-modulates-rotenone-induced-nigrostriatal-neuronal-death-and-angiogenesis-via-targeting-ampk-foxo3-transcription-factor-o3-signaling-cascade/