4.7 Article

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

Journal

JOURNAL OF ETHNOPHARMACOLOGY
Volume 208, Issue -, Pages 214-224

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/j.jep.2017.07.006

Keywords

Polysaccharides; Dendrobium officinale Kimura & Migo; Gastric injury; Oxidative damage; Apoptosis

Funding

  1. State Key Laboratory of Phytochemistry and Plant Resources in West China

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Ethnopharmacological 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 Box expression and upregulated Bcl2 expression in cell model. Further study revealed that pretreatment of DOP inhibited p-NF-kappa Bp65/NF-kappa Bp65 level, indicating DOP inhibited H2O2-mediated apoptosis via suppression of NF-kappa B 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

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