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

  • Bae, Minkyung (Department of Food and Nutrition, Brain Korea 21 PLUS Project, College of Human Ecology, Yonsei University) ;
  • Jang, Sungil (Department of Oral Biology, Oral Cancer Research Institute, Brain Korea 21 Project, Yonsei University, College of Dentistry) ;
  • Lim, Joo Weon (Department of Food and Nutrition, Brain Korea 21 PLUS Project, College of Human Ecology, Yonsei University) ;
  • Kang, Jieun (Department of Oral Biology, Oral Cancer Research Institute, Brain Korea 21 Project, Yonsei University, College of Dentistry) ;
  • Bak, Eun Jung (Department of Oral Biology, Oral Cancer Research Institute, Brain Korea 21 Project, Yonsei University, College of Dentistry) ;
  • Cha, Jeong-Heon (Department of Oral Biology, Oral Cancer Research Institute, Brain Korea 21 Project, Yonsei University, College of Dentistry) ;
  • Kim, Hyeyoung (Department of Food and Nutrition, Brain Korea 21 PLUS Project, College of Human Ecology, Yonsei University)
  • Received : 2013.06.24
  • Accepted : 2013.09.04
  • Published : 2014.01.15

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-${\kappa}B$. 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-$1{\beta}$, and iNOS; protein level of phospho-$I{\kappa}B{\alpha}$(which reflects the activation of NF-${\kappa}B$); and histology. As a result, RGE suppressed H. pylori-induced mRNA and protein levels of KC, IL-$1{\beta}$, and iNOS in gastric mucosa. RGE also inhibited H. pylori-induced phosphorylation of $I{\kappa}B{\alpha}$ 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 poly-morphonuclear neutrophils, intestinal metaplasia, and hyperplasia. In conclusion, RGE inhibits H. pyloriinduced gastric inflammation by suppressing induction of inflammatory mediators (KC, IL-$1{\beta}$, iNOS), MPO activity, and LPO level in H. pylori-infected gastric mucosa.

Keywords

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