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Conference Paper: Effects of Dendrobium officinale Polysaccharides in Cigarette Smoke-induced Inflammation in Human Airway Epithelial NCI-H292 Cells

TitleEffects of Dendrobium officinale Polysaccharides in Cigarette Smoke-induced Inflammation in Human Airway Epithelial NCI-H292 Cells
Authors
Issue Date2019
PublisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org/
Citation
The 24th Medical Research Conference, Hong Kong, 19 January 2019. In Hong Kong Medical Journal, 2019, v. 25 n. 1, Suppl. 1, p. 9, abstract no. 1 How to Cite?
AbstractBackground: Chronic obstructive pulmonary disease (COPD) is one of the leading causes of death worldwide, which is incurable with currently available treatments. Cigarette smoking is one of the major risk factors. Dendrobium officinale polysaccharide (DOP) is the major ingredient extracted from the Dendrobium officinale plant, which has been widely used as traditional Chinese medicine for years. This study aimed to explore the potential pharmacological effects of DOP on cigarette smoke-mediated airway inflammation. Methods: NCI-H292 cells were cultured until 80% confluent. After cell arrest, cells were treated with cigarette smoke medium (CSM) in the absence and presence of DOP. The viability of cells at varying concentrations of CSM or DOP was assessed by MTT assay respectively. Levels of pro-inflammatory marker interleukin (IL)-8 were measured by ELISA in the supernatants of treated cells. Results: NCI-H292 cells had poorer survival rate at CSM above 4%, whereas high dose of DOP did not exert any observable effect on cell viability. CSM caused IL-8 release in a concentration-dependent manner. DOP (below 2.5 microgram/ml) had no effect on IL-8 release, but high doses (5 and 10 microgram/ml) of DOP caused significant elevation of IL-8 release that was effectively blocked by antioxidant N-acetylcysteine (NAC). Moreover, low dose of DOP (0.01 microgram/ml) significantly inhibited CSM-induced IL-8 release, but high dose of DOP (10 microgram/ml) showed potentiation on CSM-induced IL-8 release. Conclusions: DOP demonstrated biphasic responses with inhibition of CSM-induced IL-8 release at low dose and potentiation of CSM-induced IL-8 release at high dose. These findings suggest a narrow therapeutic range of DOP as an anti-inflammatory agent in airway cells. Acknowledgement: This study was supported by Seed Fund for Basic Research of University of Hong Kong and Health & Medical Research Fund (15161911).
DescriptionOrganizer: Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong
Persistent Identifierhttp://hdl.handle.net/10722/274149
ISSN
2021 Impact Factor: 1.256
2020 SCImago Journal Rankings: 0.357

 

DC FieldValueLanguage
dc.contributor.authorAu, YNE-
dc.contributor.authorLiang, Y-
dc.contributor.authorIp, MSM-
dc.contributor.authorZhang, Y-
dc.contributor.authorMak, JCW-
dc.date.accessioned2019-08-18T14:56:03Z-
dc.date.available2019-08-18T14:56:03Z-
dc.date.issued2019-
dc.identifier.citationThe 24th Medical Research Conference, Hong Kong, 19 January 2019. In Hong Kong Medical Journal, 2019, v. 25 n. 1, Suppl. 1, p. 9, abstract no. 1-
dc.identifier.issn1024-2708-
dc.identifier.urihttp://hdl.handle.net/10722/274149-
dc.descriptionOrganizer: Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Hong Kong-
dc.description.abstractBackground: Chronic obstructive pulmonary disease (COPD) is one of the leading causes of death worldwide, which is incurable with currently available treatments. Cigarette smoking is one of the major risk factors. Dendrobium officinale polysaccharide (DOP) is the major ingredient extracted from the Dendrobium officinale plant, which has been widely used as traditional Chinese medicine for years. This study aimed to explore the potential pharmacological effects of DOP on cigarette smoke-mediated airway inflammation. Methods: NCI-H292 cells were cultured until 80% confluent. After cell arrest, cells were treated with cigarette smoke medium (CSM) in the absence and presence of DOP. The viability of cells at varying concentrations of CSM or DOP was assessed by MTT assay respectively. Levels of pro-inflammatory marker interleukin (IL)-8 were measured by ELISA in the supernatants of treated cells. Results: NCI-H292 cells had poorer survival rate at CSM above 4%, whereas high dose of DOP did not exert any observable effect on cell viability. CSM caused IL-8 release in a concentration-dependent manner. DOP (below 2.5 microgram/ml) had no effect on IL-8 release, but high doses (5 and 10 microgram/ml) of DOP caused significant elevation of IL-8 release that was effectively blocked by antioxidant N-acetylcysteine (NAC). Moreover, low dose of DOP (0.01 microgram/ml) significantly inhibited CSM-induced IL-8 release, but high dose of DOP (10 microgram/ml) showed potentiation on CSM-induced IL-8 release. Conclusions: DOP demonstrated biphasic responses with inhibition of CSM-induced IL-8 release at low dose and potentiation of CSM-induced IL-8 release at high dose. These findings suggest a narrow therapeutic range of DOP as an anti-inflammatory agent in airway cells. Acknowledgement: This study was supported by Seed Fund for Basic Research of University of Hong Kong and Health & Medical Research Fund (15161911).-
dc.languageeng-
dc.publisherHong Kong Academy of Medicine Press. The Journal's web site is located at http://www.hkmj.org/-
dc.relation.ispartofHong Kong Medical Journal-
dc.relation.ispartof24th Medical Research Conference-
dc.rightsHong Kong Medical Journal. Copyright © Hong Kong Academy of Medicine Press.-
dc.titleEffects of Dendrobium officinale Polysaccharides in Cigarette Smoke-induced Inflammation in Human Airway Epithelial NCI-H292 Cells-
dc.typeConference_Paper-
dc.identifier.emailLiang, Y: winniell@hku.hk-
dc.identifier.emailIp, MSM: msmip@hku.hk-
dc.identifier.emailZhang, Y: ybzhang@hku.hk-
dc.identifier.emailMak, JCW: judithmak@hku.hk-
dc.identifier.authorityIp, MSM=rp00347-
dc.identifier.authorityZhang, Y=rp01410-
dc.identifier.authorityMak, JCW=rp00352-
dc.identifier.hkuros301014-
dc.identifier.volume25-
dc.identifier.issue1, Suppl. 1-
dc.identifier.spage9-
dc.identifier.epage9-
dc.publisher.placeHong Kong-
dc.identifier.issnl1024-2708-

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