Red ginseng extract inhibits the expression of MCP-1 and iNOS in Helicobacter pylori-infected gastric epithelial cells by suppressing the activation of NADPH oxidase and Jak2/Stat3.
BACKGROUND
Helicobacter pylori induced oxidative stress represents an important mechanism leading to expression of inflammatory mediators. Korean red ginseng is used in traditional medicine to inhibit inflammation. However, the anti-inflammatory mechanism of red ginseng is still under investigation. Thus, we investigated whether Korean red ginseng extract (RGE) inhibits NADPH oxidase, a source of reactive oxygen species (ROS), and the Jak2/Stat3 pathway, which mediates the expression of inflammatory mediators, in Helicobacter pylori-infected gastric epithelial cells.


METHODS
A standardized RGE was supplied by the Korea Ginseng Corporation. Human gastric epithelial cells (AGS) were treated with RGE and stimulated with Helicobacter pylori. NADPH oxidase activity, ROS levels, activation of Jak2/Stat3, and induction of MCP-1 and iNOS were determined.


RESULTS
Helicobacter pylori infection resulted in an increase in ROS and activation of NADPH oxidase and Jak2/Stat3, which induced the expression of MCP-1 and iNOS in AGS cells. The induction of MCP-1 and iNOS was inhibited by both the Jak2/Stat3 inhibitor AG490 and RGE in Helicobacter pylori-infected cells. RGE suppressed NADPH oxidase activity by inhibiting translocation of cytosolic subunits p67phox and p47phox to the membrane and reduced ROS levels in Helicobacter pylori-infected cells.


CONCLUSIONS
RGE inhibits the expression of MCP-1 and iNOS by suppressing the activation of NADPH oxidase and Jak2/Stat3 in Helicobacter pylori-infected gastric epithelial cells.
Department of Food and Nutrition, Brain Korea 21 PLUS Project, College of Human Ecology, Yonsei University, Seoul 120-749, Republic of Korea.
Soon Ok
SO
Cho
Joo Weon
JW
Lim
Hyeyoung
H
Kim
D002460:Cell Line; D018932:Chemokine CCL2 / Q000037:antagonists & inhibitors* / Q000235:genetics; D004847:Epithelial Cells / Q000187:drug effects* / Q000378:metabolism; D005753:Gastric Mucosa / Q000166:cytology; D016481:Helicobacter Infections / Q000378:metabolism*; D016480:Helicobacter pylori; D006801:Humans; D053614:Janus Kinase 2 / Q000378:metabolism; D019255:NADPH Oxidases / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000037:antagonists & inhibitors* / Q000235:genetics; D005894:Panax; D010936:Plant Extracts / Q000494:pharmacology*; D017382:Reactive Oxygen Species / Q000378:metabolism; D050796:STAT3 Transcription Factor / Q000378:metabolism
C111835:CCL2 protein, human; D018932:Chemokine CCL2; D010936:Plant Extracts; D017382:Reactive Oxygen Species; D050796:STAT3 Transcription Factor; C494086:STAT3 protein, human; C496319:NOS2 protein, human; D052247:Nitric Oxide Synthase Type II; D019255:NADPH Oxidases; C507924:JAK2 protein, human; D053614:Janus Kinase 2
Gastric epithelial cells; Helicobacter pylori; MCP-1; Panax ginseng C.A. Meyer; Red ginseng extract (RGE); iNOS