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Protective effect of Korean Red Ginseng extract against Helicobacter pylori-induced gastric inflammation in Mongolian gerbils

Authors
 Minkyung Bae  ;  Sungil Jang  ;  Joo Weon Lim  ;  Jieun Kang  ;  Eun Jung Bak  ;  Jeong-Heon Cha  ;  Hyeyoung Kim 
Citation
 JOURNAL OF GINSENG RESEARCH, Vol.38(1) : 8-15, 2014 
Journal Title
 JOURNAL OF GINSENG RESEARCH 
ISSN
 1226-8453 
Issue Date
2014
Keywords
Helicobacter pylori ; Korean Red Ginseng extract ; Mongolian gerbil ; gastric inflammation
Abstract
Helicobacter pylori-induced gastric inflammation includes induction of inflammatory mediators interleukin (IL)-8 and inducible nitric oxide synthase (iNOS), which are mediated by oxidant-sensitive transcription factor NF-κB. High levels of lipid peroxide (LPO) and increased activity of myeloperoxidase (MPO), a biomarker of neutrophil infiltration, are observed in H. pylori-infected gastric mucosa. Panax ginseng Meyer, a Korean herb medicine, is widely used in Asian countries for its biological activities including anti-inflammatory efficacy. The present study aims to investigate whether Korean Red Ginseng extract (RGE) inhibits H. pylori-induced gastric inflammation in Mongolian gerbils. One wk after intragastric inoculation with H. pylori, Mongolian gerbils were fed with either the control diet or the diet containing RGE (200 mg RGE/gerbil) for 6 wk. The following were determined in gastric mucosa: the number of viable H. pylori in stomach; MPO activity; LPO level; mRNA and protein levels of keratinocyte chemoattractant factor (KC, a rodent IL-8 homolog), IL-1β, and iNOS; protein level of phospho-IκBα (which reflects the activation of NF-κB); and histology. As a result, RGE suppressed H. pylori-induced mRNA and protein levels of KC, IL-1β, and iNOS in gastric mucosa. RGE also inhibited H. pylori-induced phosphorylation of IκBα and increases in LPO level and MPO activity of gastric mucosa. RGE did not affect viable H. pylori colonization in the stomach, but improved the histological grade of infiltration of polymorphonuclear neutrophils, intestinal metaplasia, and hyperplasia. In conclusion, RGE inhibits H. pylori-induced gastric inflammation by suppressing induction of inflammatory mediators (KC, IL-1β, iNOS), MPO activity, and LPO level in H. pylori-infected gastric mucosa.
Files in This Item:
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DOI
10.1016/j.jgr.2013.11.005
Appears in Collections:
5. Research Institutes (연구소) > Oral Cancer Research Institute (구강종양연구소) > 1. Journal Papers
2. College of Dentistry (치과대학) > Dept. of Oral Biology (구강생물학교실) > 1. Journal Papers
Yonsei Authors
Kang, Ji Eun(강지은)
Bak, Eun-Jung(박은정) ORCID logo https://orcid.org/0000-0002-7976-8594
Jang, Sungil(장성일) ORCID logo https://orcid.org/0000-0001-6144-6899
Cha, Jung Heon(차정헌) ORCID logo https://orcid.org/0000-0002-9385-2653
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/97999
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