The Neuro-Protective Effect of the Methanolic Extract of Perilla frutescens var. japonica and Rosmarinic Acid against H2O2-Induced Oxidative Stress in C6 Glial Cells.
10.4062/biomolther.2015.135
- Author:
Ah Young LEE
1
;
Ting Ting WU
;
Bo Ra HWANG
;
Jaemin LEE
;
Myoung Hee LEE
;
Sanghyun LEE
;
Eun Ju CHO
Author Information
1. Department of Food Science and Nutrition & Kimchi Research Institute, Pusan National University, Busan 46241, Republic of Korea. slee@cau.ac.kr
- Publication Type:Original Article
- Keywords:
Perilla frutescens var. japonica;
Rosmarinic acid;
Oxidative stress;
Hydrogen peroxide;
C6 glial cell
- MeSH:
Cell Survival;
Cyclooxygenase 2;
Hydrogen Peroxide;
Lipid Peroxidation;
Methanol*;
Neurodegenerative Diseases;
Neuroglia*;
Neurons;
Nitric Oxide Synthase Type II;
Oxidative Stress*;
Perilla frutescens*;
Perilla*
- From:Biomolecules & Therapeutics
2016;24(3):338-345
- CountryRepublic of Korea
- Language:English
-
Abstract:
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 (H2O2) in C6 glial cells. Exposure of C6 glial cells to H2O2 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 H2O2-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 H2O2-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.
