Geraniol Protects Against the Protein and Oxidative Stress Induced by Rotenone in an In Vitro Model of Parkinson’s Disease

Aug 25, 2018Neurochemical research

Geraniol Protects Brain Cells from Protein and Oxidative Stress Caused by Rotenone in a Parkinson’s Disease Model

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Abstract

Geraniol pre-treatment enhanced cell viability by reducing rotenone-induced oxidative stress in SK-N-SH cells.

Mitochondrial dysfunction and ER stress are linked to the death of dopaminergic cells in Parkinson's disease.
Rotenone selectively induces cell death in dopaminergic neurons through multiple mechanisms.
Geraniol improved mitochondrial function by preserving membrane potential and increasing mitochondrial complex-1 levels.
Pre-treatment with geraniol reduced markers of autophagy and decreased α-synuclein expression, suggesting reduced ER stress.
The findings indicate that geraniol may provide neuroprotective effects in conditions of oxidative stress.

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Dysfunction of autophagy, mitochondrial dynamics and endoplasmic reticulum (ER) stress are currently considered as major contributing factors in the pathogenesis of Parkinson's disease (PD). Accumulation of oxidatively damaged cytoplasmic organelles and unfolded proteins in the lumen of the ER causes ER stress and it is associated with dopaminergic cell death in PD. Rotenone is a pesticide that selectively kills dopaminergic neurons by a variety of mechanism, has been implicated in PD. Geraniol (GE; 3,7-dimethylocta-trans-2,6-dien-1-ol) is an acyclic monoterpene alcohol occurring in the essential oils of several aromatic plants. In this study, we investigated the protective effect of GE on rotenone-induced mitochondrial dysfunction dependent oxidative stress leads to cell death in SK-N-SH cells. In addition, we assessed the involvement of GE on rotenone-induced dysfunction in autophagy machinery via α-synuclein accumulation induced ER stress. We found that pre-treatment of GE enhanced cell viability, ameliorated intracellular redox, preserved mitochondrial membrane potential and improves the level of mitochondrial complex-1 in rotenone treated SK-N-SH cells. Furthermore, GE diminishes autophagy flux by reduced autophagy markers, and decreases ER stress by reducing α-synuclein expression in SK-N-SH cells. Our results demonstrate that GE possess its neuroprotective effect via reduced rotenone-induced oxidative stress by enhanced antioxidant status and maintain mitochondrial function. Furthermore, GE reduced ER stress and improved autophagy flux in the neuroblastomal SK-N-SH cells. The present study could suggest that GE a novel therapeutic avenue for clinical intervention in neurodegenerative diseases especially for PD.

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Geraniol Protects Against the Protein and Oxidative Stress Induced by Rotenone in an In Vitro Model of Parkinson’s Disease

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