Study2014Open access

β-Amyloid1-42, HIV-1Ba-L (clade B) infection and drugs of abuse induced degeneration in human neuronal cells and protective effects of ashwagandha (Withania somnifera) and its constituent Withanolide A

Kurapati KR, Samikkannu T, Atluri VS, Kaftanovskaya E, Yndart A, Nair MP

PloS one · 24 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 (R01DA021537); National Institute on Drug Abuse (R37DA025576); National Institute on Drug Abuse (1R037DA025576); 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
2014-11-21 · PLoS One · vol. 9 · issue 11 · p. e112818
Publisher
Public Library of Science
Cited
37 citations · more than 98% of similar papers · 12.2× the field average
Impact
Top 10% most cited in its field
References
58 works
Access
Open access (journal) · CC-BY
Research areas
Phytochemicals and Medicinal Plants · Medicinal Plants and Neuroprotection · Alzheimer's disease research and treatments
Keywords
Withania somnifera, Pharmacology, Neuroprotection, MTT assay, Toxicity, Chemistry, Biology, Medicine, Biochemistry, Pathology, Internal medicine, Cell
MeSH
neurons, cell line, humans, hiv-1, withania, peptide fragments, neuroprotective agents, withanolides, amyloid beta-peptides, illicit drugs

6 authors

From US

  • Kesava Rao Venkata KurapatiFlorida International University
  • Thangavel SamikkannuFlorida International University
  • Venkata Subba Rao AtluriFlorida International University
  • Elena M. KaftanovskayaFlorida International University
  • Adriana YndartFlorida 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. Withania somnifera (WS) also known as 'ashwagandha' (ASH) is used widely in Ayurvedic medicine as a nerve tonic and memory enhancer. However, there is paucity of data on potential neuroprotective effects of ASH against β-Amyloid (1-42) (Aβ) induced neuropathogenesis. In the present study, we have tested the neuroprotective effects of Methanol: Chloroform (3:1) extract of ASH and its constituent Withanolide A (WA) against Aβ induced toxicity, HIV-1(Ba-L) (clade B) infection and the effects of drugs of abuse using a human neuronal SK-N-MC cell line. Aβ when tested individually, induced cytotoxic effects in SK-N-MC cells as shown by increased trypan blue stained cells. However, when ASH was added to Aβ treated cells the toxic effects were neutralized. This observation was supported by cellular localization of Aβ, MTT formazan exocytosis, and the levels of acetylcholinesterase activity, confirming the chemopreventive or protective effects of ASH against Aβ induced toxicity. Further, the levels of MAP2 were significantly increased in cells infected with HIV-1(Ba-L) (clade B) as well as in cells treated with Cocaine (COC) and Methamphetamine (METH) compared with control cells. In ASH treated cells the MAP2 levels were significantly less compared to controls. Similar results were observed in combination experiments. Also, WA, a purified constituent of ASH, showed same pattern using MTT assay as a parameter. These results suggests that neuroprotective properties of ASH observed in the present study may provide some explanation for the ethnopharmacological uses of ASH in traditional medicine for cognitive and other HIV associated neurodegenerative disorders and further ASH could be a potential novel drug to reduce the brain amyloid burden and/or improve the HIV-1 associated neurocognitive impairments.

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

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