Users Online: 775

Home Print this page Email this page Small font sizeDefault font sizeIncrease font size

Home | About us | Editorial board | Search | Ahead of print | Current issue | Archives | Submit article | Instructions | Subscribe | Contacts | Login 
Year : 2021  |  Volume : 11  |  Issue : 2  |  Page : 137-147

Neuroprotective Effect of Tephrosia purpurea Against Mitochondrial Dysfunction by Regulation of the Caspase3/9 and Pink1/Parkin Complexes

Neuroscience Laboratory, Centre for Molecular and Nanomedical Sciences, School of Bio and Chemical Engineering, Sathyabama Institute of Science and Technology, Chennai, Tamil Nadu, India

Correspondence Address:
Rajaretinam Rajesh Kannan
Centre for Molecular and Nanomedical Sciences, Sathyabama Institute of Science and Technology, Chennai 600119, Tamil Nadu
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/ijnpnd.ijnpnd_1_21

Rights and Permissions

Background: Tephrosia pupurea is a perennial shrub that has been widely incorporated in Indian traditional medicine for its anti-inflammatory and hepatoprotective effects. Recent studies have identified T. purpurea as a source of acetylcholine esterase inhibitors. Aim: In this study, we have established the potential of T. purpurea as a potential source of drugs against Parkinsonism using an oxidopamine (6-OHDA) model. Methods: Metabolomics profiling of T. purpurea extract (TPE) was obtained using the HR-LCMS method. Enzymatic activities of Catalase, Glutathione, Superoxide Dismutase and Malondialdehyde were measured in vitro. Reactive Oxygen Species generation capacity and the mitochondrial membrane potential were also determined. The zebrafish embryos were treated with oxidopamine along with varying concentrations of T. purpurea extract and the swimming pattern and total distance travelled was evaluated. The mRNA expression of mitophagy related genes were measured using RT-PCR studies. Results: The metabolite profile of T. purpurea identified the presence of various polyphenols such as Genistein, Esculetin, and Chrysin that have neuroprotective effects. 6-OHDA-induced PD causes an increase in oxidative stress, reactive oxygen species generation, and affects mitochondrial stability. There was a significant increase in the catalase, glutathione, and superoxide dismutase levels and a decrease in Malondialdehyde and Reactive Oxygen Species levels in cells treated with TPE when compared to 6-OHDA treated cells. We then treated zebrafish embryos with 6-OHDA along with varying concentrations of T. purpurea extract, and the mRNA expression and swimming pattern were evaluated. The embryos cotreated with TPE showed improved swim pattern similar to untreated embryos, whereas those treated with the positive control failed to do so. T. purpurea extract also significantly decreased the expressions of casp3, casp9, lrrk2, and increased pink1 and parkin expression. Conclusion: Our study identifies Tephrosia purpurea extract as a viable candidate against 6-OHDA induced-neurotoxicity, and further studies of its effect in models of neurodegenerative diseases are required.

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
    PDF Downloaded122    
    Comments [Add]    

Recommend this journal