Evaluation of the Mitochondria-Related Redox and Bioenergetics Effects of Gastrodin in SH-SY5Y Cells Exposed to Hydrogen Peroxide

• Published in: Journal of molecular neuroscience 2018-02, Vol.64 (2), p.242-251
• Main Authors: de Oliveira, Marcos Roberto, Brasil, Flávia Bittencourt, Fürstenau, Cristina Ribas
• Format: Article
• Language: English
• Subjects: Adenosine Triphosphate - metabolism; Alcohols; Antioxidants; Antioxidants - pharmacology; Benzyl Alcohols - pharmacology; Bioenergetics; Biomedical and Life Sciences; Biomedicine; Blood-brain barrier; Cardiovascular diseases; Cell Biology; Cell death; Cell Line, Tumor; Cell survival; Cognition; Glucosides - pharmacology; Herbal medicine; Humans; Hydrogen peroxide; Hydrogen Peroxide - toxicity; Impairment; Inflammation; Mitochondria; Mitochondria - drug effects; Mitochondria - metabolism; Neuroblasts; Neurochemistry; Neurodegeneration; Neurology; Neurosciences; NF-E2-Related Factor 2 - metabolism; Oxidation-Reduction; Pharmacology; Phenolic compounds; Phenols; Proteomics; Redox properties; Signaling
• ISSN: 0895-8696; 1559-1166
• DOI: 10.1007/s12031-018-1027-0

Mitochondrion is the main site of ATP production in animal cells and also orchestrates signaling pathways associated with cell survival and death. Mitochondrial dysfunction has been linked to bioenergetics and redox impairment in human diseases, such as neurodegeneration and cardiovascular disease. Protective agents able to attenuate mitochondrial impairment are of pharmacological interest. Gastrodin (GAS; 4-hydroxybenzyl alcohol 4-O-beta- d -glucoside) is a phenolic glucoside obtained from the Chinese herbal medicine Gastrodia elata Blume and exhibits antioxidant, anti-inflammatory, and antiapoptotic effects in several cell types. GAS is able to cross the blood-brain barrier, reducing the impact of different stressors on the cognition of experimental animals. In the present work, we investigated whether GAS would protect mitochondria of human SH-SY5Y neuroblastoma cells against an exposure to a pro-oxidant agent. The cells were treated with GAS at 25 μM for 30 min before the administration of hydrogen peroxide (H 2 O 2 ) at 300 μM for an additional 3 or 24 h, depending on the assay. We evaluated both mitochondrial redox state and function parameters and analyzed the mechanism by which GAS protected mitochondria in this experimental model. Silencing of the nuclear factor erythroid 2-related factor 2 (Nrf2) transcription factor suppressed the GAS-induced mitochondrial protection seen here. Moreover, Nrf2 knockdown abrogated the effects of GAS on cell viability, indicating a potential role for Nrf2 in both mitochondrial and cellular protection promoted by GAS. Further research would be necessary to investigate whether GAS would be able to induce similar effects in in vivo experimental models.