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Conference Paper: Plant Natural Product Puerarin Ameliorates Depressive Behaviors and Chronic Pain in Mice with Spared Nerve Injury (SNI)

TitlePlant Natural Product Puerarin Ameliorates Depressive Behaviors and Chronic Pain in Mice with Spared Nerve Injury (SNI)
Authors
Issue Date2016
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NED
Citation
New Zealand Applied Neurosciences Conference 2016, Auckland, New Zealand, 24-26 November 2016. Abstracts in Neuroepidemiology, 2016, v. 47 n. 3-4, p. 139, abstract no. 402 How to Cite?
AbstractSimultaneous relief of the pain from body and brain remains an ongoing challenge. The aim of the present study was to clarify whether plant-derived isoflavone puerarin could ameliorate comorbid depression and pain. We investigated the effects of puerarin on depressive-like behaviors and neuropathic pain in C57BL/6N mice with spared nerve injury (SNI). After SNI surgery, mice were allowed to recover spontaneously for 7 days and subsequently treated with puerarin, anti-depressant citalopram, and analgesic ibuprofen, alone or in combination, for 8 or 14 days. Forced swim test and tail suspension test were used to assess depressive-like behaviors, whereas von Frey filament test was used to estimate the sensitivity to the mechanical stimulation. Our results suggested that puerarin effectively ameliorated depression and pain in SNI mice although citalopram exhibited anti-depressant activity. In contrast, ibuprofen showed lesser activities against SNI-induced depression and pain. Further mechanistic studies revealed the uniqueness of puerarin as follows: (1) puerarin did not recover SNI-induced depletion of reduced glutathione and loss of superoxide dismutase (SOD), whereas citalopram and ibuprofen showed somewhat antioxidant activities; (2) puerarin markedly promoted the activation of CREB pathway although puerarin and citalopram activated ERK pathway to the same extent; (3) puerarin rapidly and persistently induced brain-derived neurotrophic factor (BDNF) expression whereas citalopram only induced BDNF expression after a prolonged stimulation. Collectively, these results suggest that puerarin may ameliorate the SNI-induced depression and pain via activating ERK, CREB, and BDNF pathways. Puerarin may serve as new lead compound for the development of novel therapeutics for depression and pain comorbidity.
DescriptionPoster Presentation - Session P2 – Basic Neuroscience Research - no. 402
Persistent Identifierhttp://hdl.handle.net/10722/246393
ISSN
2019 Impact Factor: 2.186
2015 SCImago Journal Rankings: 1.726

 

DC FieldValueLanguage
dc.contributor.authorZhao, J-
dc.contributor.authorLao, L-
dc.contributor.authorRong, J-
dc.date.accessioned2017-09-18T02:27:44Z-
dc.date.available2017-09-18T02:27:44Z-
dc.date.issued2016-
dc.identifier.citationNew Zealand Applied Neurosciences Conference 2016, Auckland, New Zealand, 24-26 November 2016. Abstracts in Neuroepidemiology, 2016, v. 47 n. 3-4, p. 139, abstract no. 402-
dc.identifier.issn0251-5350-
dc.identifier.urihttp://hdl.handle.net/10722/246393-
dc.descriptionPoster Presentation - Session P2 – Basic Neuroscience Research - no. 402-
dc.description.abstractSimultaneous relief of the pain from body and brain remains an ongoing challenge. The aim of the present study was to clarify whether plant-derived isoflavone puerarin could ameliorate comorbid depression and pain. We investigated the effects of puerarin on depressive-like behaviors and neuropathic pain in C57BL/6N mice with spared nerve injury (SNI). After SNI surgery, mice were allowed to recover spontaneously for 7 days and subsequently treated with puerarin, anti-depressant citalopram, and analgesic ibuprofen, alone or in combination, for 8 or 14 days. Forced swim test and tail suspension test were used to assess depressive-like behaviors, whereas von Frey filament test was used to estimate the sensitivity to the mechanical stimulation. Our results suggested that puerarin effectively ameliorated depression and pain in SNI mice although citalopram exhibited anti-depressant activity. In contrast, ibuprofen showed lesser activities against SNI-induced depression and pain. Further mechanistic studies revealed the uniqueness of puerarin as follows: (1) puerarin did not recover SNI-induced depletion of reduced glutathione and loss of superoxide dismutase (SOD), whereas citalopram and ibuprofen showed somewhat antioxidant activities; (2) puerarin markedly promoted the activation of CREB pathway although puerarin and citalopram activated ERK pathway to the same extent; (3) puerarin rapidly and persistently induced brain-derived neurotrophic factor (BDNF) expression whereas citalopram only induced BDNF expression after a prolonged stimulation. Collectively, these results suggest that puerarin may ameliorate the SNI-induced depression and pain via activating ERK, CREB, and BDNF pathways. Puerarin may serve as new lead compound for the development of novel therapeutics for depression and pain comorbidity.-
dc.languageeng-
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NED-
dc.relation.ispartofNeuroepidemiology-
dc.rightsNeuroepidemiology. Copyright © S Karger AG.-
dc.titlePlant Natural Product Puerarin Ameliorates Depressive Behaviors and Chronic Pain in Mice with Spared Nerve Injury (SNI)-
dc.typeConference_Paper-
dc.identifier.emailZhao, J: zhaojia7@hku.hk-
dc.identifier.emailLao, L: lxlao1@hku.hk-
dc.identifier.emailRong, J: jrong@hku.hk-
dc.identifier.authorityLao, L=rp01784-
dc.identifier.authorityRong, J=rp00515-
dc.identifier.hkuros276302-
dc.identifier.volume47-
dc.identifier.issue3-4-
dc.identifier.spage139, abstract no. 402-
dc.identifier.epage139, abstract no. 402-
dc.publisher.placeSwitzerland-

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