2020-05-04 11:51:17 +02:00
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<title classid="main title" classname="main title" schemeid="dnet:dataCite_title"
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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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schemename="dnet:access_modes"/>
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<creator rank="1">Jain, Subhash C.</creator>
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<creator rank="2">Citron, Bruce A.</creator>
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<creator rank="3">Vijayalakshmi Ravindranath</creator>
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<creator rank="4">Saykally, Jessica N.</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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2021-02-12 12:31:02 +01:00
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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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2020-05-04 11:51:17 +02:00
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<dateofacceptance>2017-06-01</dateofacceptance>
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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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schemename="dnet:subject_classification_typologies" inferred="false">Withania
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somnifera</subject>
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>neuroprotection</subject>
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schemename="dnet:subject_classification_typologies" inferred="false">traumatic
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brain injury</subject>
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<relevantdate classid="dnet:date" classname="dnet:date" schemeid="dnet:date"
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schemename="dnet:date" inferred="false">2018-11-13</relevantdate>
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>2017-7-1</relevantdate>
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<publisher>SAGE Publishing</publisher>
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<source>Cell Transplantation, Vol 26 (2017)</source>
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<source>Cell Transplantation</source>
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2021-02-12 12:31:02 +01:00
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2020-05-04 11:51:17 +02:00
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<journal issn="0963-6897" eissn="1555-3892" ep="1201" iss="7" sp="1193" vol="26"
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>Cell Transplantation</journal>
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confidenceLevel="0.9"/>
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<id value="24458838" type="pmid" confidenceLevel="0.9"/>
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</citation>
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|
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</citations>
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</extraInfo>
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</oaf:entity>
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</metadata>
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</result>
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