Study2013Open access

Ashwagandha (Withania somnifera) reverses β-amyloid1-42 induced toxicity in human neuronal cells: implications in HIV-associated neurocognitive disorders (HAND)

Kurapati KR, Atluri VS, Samikkannu T, Nair MP

PloS one · 73 citations

Review labels

Mechanisms only

Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.

How it was studied

Design
In vitro/mechanistic study (classified by our AI screen)
Studied in
Cells or lab samples
Main outcome
Mechanisms only

Who paid for it

Funding
Independent funding
Government
National Institute of Mental Health
Government
National Institute on Drug Abuse
Government
NIMH NIH HHS
Government
NIDA NIH HHS
Grants
National Institute on Drug Abuse (1R01-DA027049); National Institute on Drug Abuse (1R37DA025576); National Institute on Drug Abuse (R01DA021537); National Institute on Drug Abuse (R37DA025576); National Institute of Mental Health (R01 MH085259); National Institute on Drug Abuse (5R01DA021537); National Institute of Mental Health (1R01MH085259); National Institute on Drug Abuse (R01-DA027049)

Based on 4 listed funder(s) and full-text disclosure statement.

Publication

Published
2013-10-16 · PLoS One · vol. 8 · issue 10 · p. e77624
Publisher
Public Library of Science
Cited
129 citations · more than 100% of similar papers · 28.3× the field average
Impact
Top 10% most cited in its field
References
75 works
Access
Open access (journal) · CC-BY
Research areas
Phytochemicals and Medicinal Plants · Medicinal Plants and Neuroprotection
Keywords
Withania somnifera, Neurocognitive, Toxicity, Neurotoxicity, Biology, Medicine, Pharmacology, Neuroscience, Pathology, Internal medicine, Cognition
MeSH
neurons, dendrites, cell line, humans, withania, hiv infections, nervous system diseases, hydro-lyases, peptide fragments, ppar gamma, neuroprotective agents, plant extracts, chromatography, high pressure liquid, cell survival, mass spectrometry, amyloid beta-peptides

4 authors

From US

  • Kesava Rao Venkata KurapatiFlorida International University
  • Venkata Subba Rao AtluriFlorida International University
  • Thangavel SamikkannuFlorida International University
  • Madhavan Nair · correspondingFlorida International University

Abstract

Alzheimer's disease (AD) is characterized by progressive dysfunction of memory and higher cognitive functions with abnormal accumulation of extracellular amyloid plaques and intracellular neurofibrillary tangles throughout cortical and limbic brain regions. At present no curative treatment is available, and research focuses on drugs for slowing disease progression or providing prophylaxis. Withania somnifera (WS) also known as 'ashwagandha' is used widely in Ayurvedic medicine as a nerve tonic and memory enhancer. However, there is a paucity of data on the potential neuroprotective effects of W.somnifera against β-Amyloid (1-42)-induced neuropathogenesis. In the present study, we have tested the neuroprotective effects of methanol:Chloroform (3:1) extract of ashwagandha against β-amyloid induced toxicity and HIV-1Ba-L (clade B) infection using a human neuronal SK-N-MC cell line. Our results showed that β-amyloid induced cytotoxic effects in SK-N-MC cells as shown by decreased cell growth when tested individually. Also, confocal microscopic analysis showed decreased spine density, loss of spines and decreased dendrite diameter, total dendrite and spine area in clade B infected SK-N-MC cells compared to uninfected cells. However, when ashwagandha was added to β-amyloid treated and HIV-1 infected samples, the toxic effects were neutralized. Further, the MTT cell viability assays and the peroxisome proliferator-activated receptor-γ (PPARγ) levels supported these observations indicating the neuroprotective effect of WS root extract against β-amyloid and HIV-1Ba-L (clade B) induced neuro-pathogenesis.

Abstract via Europe PMC. Copyright remains with the authors or publisher (CC BY).

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