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Chlorogenic Acid Exerts Beneficial Effects in 6-Hydroxydopamine-Induced Neurotoxicity by Inhibition of Endoplasmic Reticulum Stress

BACKGROUND: Chlorogenic acid (CGA), a dietary polyphenol derived from many plants, has been previously reported to exert neuroprotective properties. However, its pharmacological role in Parkinson’s disease (PD) and the underlying mechanisms are unclear. MATERIAL/METHODS: In the present study, we inv...

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Detalles Bibliográficos
Autores principales: Shan, Shihai, Tian, Lina, Fang, Ruihuan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6342059/
https://www.ncbi.nlm.nih.gov/pubmed/30645211
http://dx.doi.org/10.12659/MSM.911166
Descripción
Sumario:BACKGROUND: Chlorogenic acid (CGA), a dietary polyphenol derived from many plants, has been previously reported to exert neuroprotective properties. However, its pharmacological role in Parkinson’s disease (PD) and the underlying mechanisms are unclear. MATERIAL/METHODS: In the present study, we investigated the beneficial effects of CGA against the toxicity of 6-hydroxydopamine (6-OHDA) in animal and cellular models. One week after 6-OHDA administration, the behavioral activities of rats were determined by rotarod test and apomorphine-induced rotational test. The viability and apoptosis of SH-SY5Y cells following 6-OHDA exposure were determined by MTT assay and annexin V-FITC/PI double staining, respectively. The activities of antioxidant enzymes in the rat striatal tissues and SH-SY5Y cells were detected by ELISA. RESULTS: The results demonstrated that 6-OHDA-induced PD-like behavioral impairments of rats were significantly forestalled by CGA administration. The increased apoptosis and reduced activities of antioxidant enzymes in the striatum of 6-OHDA-lesioned rats were also attenuated by CGA. Moreover, in an in vitro experiment, the impaired viability and enhanced apoptosis of 6-OHDA-injured SH-SY5Y cells were significantly restored by CGA pretreatment. In addition, CGA also obstructed 6-OHDA-induced ROS production and endoplasmic reticulum (ER) stress in SH-SY5Y cells. CONCLUSIONS: Taken together, these data show that CGA might be an effective neuroprotective compound that mitigates oxidative stress and ER stress in PD.