Rosmarinic acid mediated neuroprotective effects against H2O2-induced neuronal cell damage in N2A cells

被引:93
|
作者
Ghaffari, Hadi [1 ]
Venkataramana, M. [2 ]
Ghassam, Behrouz Jalali [1 ]
Nayaka, S. Chandra [1 ]
Nataraju, A. [3 ]
Geetha, N. P. [1 ]
Prakash, H. S. [1 ]
机构
[1] Univ Mysore, Dept Studies Biotechnol, Mysore 570006, Karnataka, India
[2] Bharathiar Univ Campus, DRDO BU Ctr Life Sci, Coimbatore 640046, Tamil Nadu, India
[3] KSOU, Dept Biochem, Mysore 06, Karnataka, India
关键词
Rosmarinic acid; Oxidative stress; N2A cells; Neuroprotection; DNA damage; Gene expression; OXIDATIVE STRESS; MEDICINAL-PLANTS; CARNOSIC ACID; ANTIOXIDANT; APOPTOSIS; ROSEMARY;
D O I
10.1016/j.lfs.2014.07.010
中图分类号
R-3 [医学研究方法]; R3 [基础医学];
学科分类号
1001 ;
摘要
Aims: Oxidative stress plays a key role in several ailments including neurodegenerative conditions. The aim of the study was to demonstrate the effect of rosmarinic acid (RA) in preventing oxidative stress related death of neuronal cell lines. Main methods: In the present study, we demonstrated direct neuroprotective effect of RA using H2O2-induced oxidative challenge in N2A mouse neuroblastoma cells. The mechanism of neutralization of H2O2-induced toxicity by RA was evaluated using MU, lactate dehydrogenase, mitochondrial membrane potential (MMP), intracellular ROS, and comet assays. Up-regulation of brain neuronal markers at molecular level was performed by RT-PCR. Key findings: Results presented in the paper indicate that H2O2-induced cytotoxicity in N2A cells was suppressed by treatment with RA. Moreover, RA is very effective in attenuating the disruption of lactate dehydrogenase, mitochondrial membrane potential and intracellular ROS. Pretreatment with RA significantly prevents genotoxicity (3.7-fold, p < 0.01) and promotes the up-regulation of tyrosine hydroxylase (TH) (4.5-fold, p < 0.01), and brain-derived neurotrophic factor (BDNF) genes (5.4-fold, p < 0.01) against H2O2-induced cytotoxicity in N2A cells. Significance: Our results revealed that N2A cells are suitable cellular models to evaluate neuroprotective effects of RA, and suggest that RA may potentially serve as an agent for prevention of several human neurodegenerative diseases caused by oxidative stress. (C) 2014 Elsevier Inc. All rights reserved.
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页码:7 / 13
页数:7
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