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.

ETHNOPHARMCOLOGICAL RELEVANCE

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.

MATERIALS AND 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.

CONCLUSION

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.