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The Neuro-Protective Effect of the Methanolic Extract of Perilla frutescens var. japonica and Rosmarinic Acid against H(2)O(2)-Induced Oxidative Stress in C6 Glial Cells

Neurodegenerative diseases are often associated with oxidative damage in neuronal cells. This study was conducted to investigate the neuro-protective effect of methanolic (MeOH) extract of Perilla frutescens var. japonica and its one of the major compounds, rosmarinic acid, under oxidative stress in...

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Detalles Bibliográficos
Autores principales: Lee, Ah Young, Wu, Ting Ting, Hwang, Bo Ra, Lee, Jaemin, Lee, Myoung-Hee, Lee, Sanghyun, Cho, Eun Ju
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Society of Applied Pharmacology 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4859798/
https://www.ncbi.nlm.nih.gov/pubmed/27133263
http://dx.doi.org/10.4062/biomolther.2015.135
Descripción
Sumario:Neurodegenerative diseases are often associated with oxidative damage in neuronal cells. This study was conducted to investigate the neuro-protective effect of methanolic (MeOH) extract of Perilla frutescens var. japonica and its one of the major compounds, rosmarinic acid, under oxidative stress induced by hydrogen peroxide (H(2)O(2)) in C6 glial cells. Exposure of C6 glial cells to H(2)O(2) enhanced oxidative damage as measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and thiobarbituric acid-reactive substance assays. The MeOH extract and rosmarinic acid prevented oxidative stress by increasing cell viability and inhibiting cellular lipid peroxidation. In addition, the MeOH extract and rosmarinic acid reduced H(2)O(2)-induced expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) at the transcriptional level. Moreover, iNOS and COX-2 protein expression was down-regulated in H(2)O(2)-indcued C6 glial cells treated with the MeOH extract and rosmarinic acid. These findings suggest that P. frutescens var. japonica and rosmarinic acid could prevent the progression of neurodegenerative diseases through attenuation of neuronal oxidative stress.