Home | About PM | Editorial board | Search | Ahead of print | Current Issue | Archives | Instructions | Subscribe | Advertise | Contact us |  Login 
Pharmacognosy Magazine
Search Article 
  
Advanced search 
 
ORIGINAL ARTICLE
Year : 2018  |  Volume : 14  |  Issue : 57  |  Page : 458-464

Naringenin protects against 1-methyl-4-phenylpyridinium- induced neuroinflammation and resulting reactive oxygen species production in SH-SY5Y cell line: An in Vitro model of parkinson's disease


1 Research and Development Centre, Bharathiar University, Coimbatore, Tamil Nadu, India
2 Department of Biotechnology, Dr. M. G. R. Educational and Research Institute University, Chennai, Tamil Nadu, India
3 Department of Pharmacology, JSS College of Pharmacy, JSS University, Mysore, Karnataka, India
4 Department of Biotechnology, Karunya Institute of Technology and Sciences, Coimbatore, Tamil Nadu, India

Correspondence Address:
Murugan Sevanan
Department of Biotechnology, Karunya Institute of Technology and Sciences, Karunya Nagar, Coimbatore - 641 114, Tamil Nadu
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/pm.pm_23_18

Rights and Permissions

Background: Parkinson's disease is a progressive neurodegenerative disorder which affects 1% of the population worldwide. It is well known that 1-methyl-4-phenylpyridinium (MPP+) selectively and potentially inhibit Complex I of the mitochondrial electron transport chain. This inactivation leads to the generation of reactive oxygen species (ROS), which in turn damage neurons. In addition, neuroinflammation plays a major role in neurodegeneration processes. Objective: In the present study, the effect of naringenin (NGN), on MPP+-induced neuroinflammation and ROS generation in SH-SY5Y cells were investigated. Materials and Methods: Cells were pretreated with (0.1% dimethyl sulfoxide) or NGN (25, 50, and 100 μm/mL) for 24 h, and then induced with 1 mM MPP+ for 15 min. Following overnight incubation, cells were harvested for ROS staining, gene expression of apoptotic markers such as B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein (Bax), inflammatory markers such as tumor necrosis factor-alpha (TNF-α), and nuclear factor-κB (NF-κB) and protein expression of neuronal markers such as dopamine transporter (DAT), tyrosine hydroxylase (TH), and α-synuclein (SYN). Results: In this study, NGN exhibited oxidative protection by decreasing ROS generation which is evidenced through significant regulation of oxidative stress markers. Likewise, NGN decreased TNF-α, Bax, and NF-κB and increased Bcl-2 gene expressions in MPP+-induced SH-SY5Y cells compared to normal SH-SY5Y cells. Further, NGN significantly and dose-dependently decreased SYN and increased DAT and TH levels in MPP+-induced SH-SY5Y cells in comparison to the normal cells. Conclusion: The results obtained from the present study revealed that NGN has the potential to encounter MPP+-induced dopaminergic degeneration through regulating ROS generation and neuroinflammation. Abbreviations used: TNF-α: Tumor Necrosis Factor alpha; NF-κB: Nuclear factor; SYN-α: synuclein; NGN: Naringenin; MPP+: 1-methyl-4-phenylpyridinium; MPTP: 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine; PD-Parkinson's disease; DCFH-DA: 2',7' - dichlorofluorescin diacetate; SOD: Superoxide dismutase; NO: Nitric oxide; MDA: Malondialdehyde; DAT: Dopamine transporter; TH: Tyrosine hydroxylase; ANOVA: Analysis of variance; SEM: Standard error of the mean; RT-PCR: Reverse transcriptase-polymerase chain reaction; BSA: Bovine serum albumin; PBS: Phosphate buffered saline; TBST: Tris-Buffered saline with Tween; RNA: Ribonucleic acid.


[FULL TEXT] [PDF]*
Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)
 

 Article Access Statistics
    Viewed386    
    Printed18    
    Emailed0    
    PDF Downloaded5    
    Comments [Add]    

Recommend this journal