The neuroprotective effects of hydro-alcoholic extract of olive (Olea europaea L.) leaf on rotenone-induced Parkinson’s disease in rat

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Abstract

Parkinson’s disease (PD) is an age-related disease in which dopaminergic neurons in the nigrostriatal pathway are destroyed, resulting in movement and behavioral problems. Oxidative stress and the generation of reactive oxygen species play key roles in neurodegenerative diseases, such as PD. Rotenone (ROT) is a common pesticide that induces oxidative stress. Olive leaves extract (OLE) has antioxidant and neuroprotective effects. Thus, the aim of this study was to investigate the neuroprotective effects of OLE on ROT-induced oxidative stress in the midbrain of a rat model of PD. Ninety-six Wistar rats were randomly divided into the following 6 groups (n = 16 rats/group): Control, Sham, ROT, and 3 ROT + OLE (75, 150, and 300 mg/kg/daily) groups. ROT (2.5 mg/kg/48 h) was injected subcutaneously, and vehicle or OLE was orally administered for 30 days. The animals were then sacrificed, and their brains were removed. Biochemical measures, including the levels of catalase (CAT), glutathione peroxidase (GPx), superoxide dismutase (SOD), and malondialdehyde (MDA), and the number of tyrosine hydroxylase (TH)-positive neurons were determined, and behavioral (rotarod and hanging) tests were conducted. The balance and muscle strength of the OLE (150 and 300 mg/kg)-treated groups were significantly improved. Treatment with OLE prevented the increases in the levels of MDA, significantly improved the SOD, CAT, and GPx levels in the midbrain, and prevented the depletion of the TH-positive neurons. These findings suggested that OLE has neuroprotective properties and that it might be useful for preventing the death of dopaminergic neurons in patients with PD.

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Sarbishegi, M., Charkhat Gorgich, E. A., Khajavi, O., Komeili, G., & Salimi, S. (2018). The neuroprotective effects of hydro-alcoholic extract of olive (Olea europaea L.) leaf on rotenone-induced Parkinson’s disease in rat. Metabolic Brain Disease, 33(1), 79–88. https://doi.org/10.1007/s11011-017-0131-0

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