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Article: Polysaccharides of Dendrobium officinale Kimura & Migo protect gastric mucosal cell against oxidative damage-induced apoptosis in vitro and in vivo

TitlePolysaccharides of Dendrobium officinale Kimura & Migo protect gastric mucosal cell against oxidative damage-induced apoptosis in vitro and in vivo
Authors
KeywordsApoptosis
Dendrobium officinale Kimura & Migo
Gastric injury
Oxidative damage
Polysaccharides
Issue Date2017
Citation
Journal of Ethnopharmacology, 2017, v. 208, p. 214-224 How to Cite?
AbstractEthnopharmacological relevance Dendrobium officinale Kimura & Migo (DO) is a valuable Traditional Chinese Medicine to nourish stomach, in which polysaccharides are identified as active ingredients. However, limited scientific evidences have been reported on the gastroprotective efficacy of DO. The aim of the current study was to investigate the protective effects and underlying mechanism of polysaccharides from DO(DOP) on gastric mucosal injury. Material and methods For in vitro study, HFE145 cells were pretreated with DOP before induction of cell apoptosis by H2O2. Cell apoptosis and related proteins expression were detected. In the in vivo study, absolute ethanol was administered orally to induce gastric mucosal injury in rat. The gastric mucosal injury area and histological examination were used to evaluate the effects of DOP treatment on the recovery of the gastric mucosal injury. Results H2O2 treatment for 6 h significantly induced cell apoptosis in HFE145 cells. However, the destructive effects of H2O2 on HFE 145 cells could be reversed by the pretreatment with DOP. The increased ROS level induced by H2O2 for 4 h was reduced after DOP pretreatment. The number of apoptotic cells in both early and late apoptosis stages decreased significantly and the nuclei morphology changes were improved with DOP pretreatment. Furthermore, DOP inhibited caspase 3 activation and PARP cleavage, downregulated Bax expression and upregulated Bcl2 expression in cell model. Further study revealed that pretreatment of DOP inhibited p -NF-κBp65/NF-κBp65 level, indicating DOP inhibited H2O2-mediated apoptosis via suppression of NF-κB activation. In addition, DOP treatment could ameliorate gastric mucosal injury and inhibit mucin loss induced by ethanol in animal model. DOP treatment also interfered with ethanol-induced apoptosis process by downregulating Bax/Bcl2 ratio in gastric mucosa. Conclusions The present study was the first one to demonstrate the gastroprotective effect of DOP through inhibiting oxidative stress-induced apoptosis. This study provided a solid evidence for the potential use of DO as a therapy or health supplement for gastric mucosal diseases
Persistent Identifierhttp://hdl.handle.net/10722/343242
ISSN
2023 Impact Factor: 4.8
2023 SCImago Journal Rankings: 0.936

 

DC FieldValueLanguage
dc.contributor.authorZeng, Qiang-
dc.contributor.authorKo, Chun Hay-
dc.contributor.authorSiu, Wing Sum-
dc.contributor.authorLi, Long Fei-
dc.contributor.authorHan, Xiao Qiang-
dc.contributor.authorYang, Liu-
dc.contributor.authorBik-San Lau, Clara-
dc.contributor.authorHu, Jiang Miao-
dc.contributor.authorLeung, Ping Chung-
dc.date.accessioned2024-05-10T09:06:33Z-
dc.date.available2024-05-10T09:06:33Z-
dc.date.issued2017-
dc.identifier.citationJournal of Ethnopharmacology, 2017, v. 208, p. 214-224-
dc.identifier.issn0378-8741-
dc.identifier.urihttp://hdl.handle.net/10722/343242-
dc.description.abstractEthnopharmacological relevance Dendrobium officinale Kimura & Migo (DO) is a valuable Traditional Chinese Medicine to nourish stomach, in which polysaccharides are identified as active ingredients. However, limited scientific evidences have been reported on the gastroprotective efficacy of DO. The aim of the current study was to investigate the protective effects and underlying mechanism of polysaccharides from DO(DOP) on gastric mucosal injury. Material and methods For in vitro study, HFE145 cells were pretreated with DOP before induction of cell apoptosis by H2O2. Cell apoptosis and related proteins expression were detected. In the in vivo study, absolute ethanol was administered orally to induce gastric mucosal injury in rat. The gastric mucosal injury area and histological examination were used to evaluate the effects of DOP treatment on the recovery of the gastric mucosal injury. Results H2O2 treatment for 6 h significantly induced cell apoptosis in HFE145 cells. However, the destructive effects of H2O2 on HFE 145 cells could be reversed by the pretreatment with DOP. The increased ROS level induced by H2O2 for 4 h was reduced after DOP pretreatment. The number of apoptotic cells in both early and late apoptosis stages decreased significantly and the nuclei morphology changes were improved with DOP pretreatment. Furthermore, DOP inhibited caspase 3 activation and PARP cleavage, downregulated Bax expression and upregulated Bcl2 expression in cell model. Further study revealed that pretreatment of DOP inhibited p -NF-κBp65/NF-κBp65 level, indicating DOP inhibited H2O2-mediated apoptosis via suppression of NF-κB activation. In addition, DOP treatment could ameliorate gastric mucosal injury and inhibit mucin loss induced by ethanol in animal model. DOP treatment also interfered with ethanol-induced apoptosis process by downregulating Bax/Bcl2 ratio in gastric mucosa. Conclusions The present study was the first one to demonstrate the gastroprotective effect of DOP through inhibiting oxidative stress-induced apoptosis. This study provided a solid evidence for the potential use of DO as a therapy or health supplement for gastric mucosal diseases-
dc.languageeng-
dc.relation.ispartofJournal of Ethnopharmacology-
dc.subjectApoptosis-
dc.subjectDendrobium officinale Kimura & Migo-
dc.subjectGastric injury-
dc.subjectOxidative damage-
dc.subjectPolysaccharides-
dc.titlePolysaccharides of Dendrobium officinale Kimura & Migo protect gastric mucosal cell against oxidative damage-induced apoptosis in vitro and in vivo-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.jep.2017.07.006-
dc.identifier.pmid28684298-
dc.identifier.scopuseid_2-s2.0-85024868917-
dc.identifier.volume208-
dc.identifier.spage214-
dc.identifier.epage224-
dc.identifier.eissn1872-7573-

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