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schemename="dnet:dataCite_title" inferred="false">Extract Protects Model Neurons
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from Traumatic Injury</title>
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<creator rank="3">Vijayalakshmi Ravindranath</creator>
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<creator rank="5">Keeley, Kristen L.</creator>
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<creator rank="6">Haris Hatic</creator>
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<creator rank="7" name="Miriam" surname="Baglioni" orcid_pending="0000-0002-2273-9004">Baglioni, Miriam</creator>
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<creator rank="8" name="Michele" surname="De Bonis" orcid="0000-0002-2273-9004">De Bonis, Michele</creator>
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<description>Withania somnifera has been used in traditional medicine for a variety
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of neural disorders. Recently, chronic neurodegenerative conditions have been
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shown to benefit from treatment with this extract. To evaluate the action of
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this extract on traumatically injured neurons, the efficacy of W. somnifera root
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extract as a neuroprotective agent was examined in cultured model neurons
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exposed to an in vitro injury system designed to mimic mild traumatic brain
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injury (TBI). Neuronal health was evaluated by staining with annexin V (an
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early, apoptotic feature) and monitoring released lactate dehydrogenase activity
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(a terminal cell loss parameter). Potential mechanisms underlying the observed
|
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neuroprotection were examined. Additionally, morphological changes were
|
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monitored following injury and treatment. Although no differences were found in
|
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|
the expression of the antioxidant transcription factor nuclear factor erythroid
|
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|
2-like 2 (Nrf2) or other Nrf2-related downstream components, significant changes
|
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were seen in apoptotic signaling. Treatment with the extract resulted in an
|
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increased length of neurites projecting from the neuronal cell body after
|
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injury. W. somnifera extract treatment also resulted in reduced cell death in
|
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the model neuron TBI system. The cell death factor Bax was involved (its
|
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expression was reduced 2-fold by the treatment) and injury-induced reduction in
|
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neurite lengths and numbers was reversed by the treatment. This all indicates
|
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that W. somnifera root extract was neuroprotective and could have therapeutic
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potential to target factors involved in secondary injury and long-term sequelae
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of mild TBI.</description>
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<source>Cell Transplantation, Vol 26 (2017)</source>
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