Standardized ginger (Zingiber officinale) extract reduces bacterial load and suppresses acute and chronic inflammation in Mongolian gerbils infected with cagAHelicobacter pylori

Abstract

Previous investigations demonstrated that a standardized extract of ginger rhizome inhibited the growth of Helicobacter pylori in vitro with a minimum inhibitory concentration in the range 0.78 to 12.5 mug/mL. In the present work, the extract was tested in a rodent model of H. pylori-induced disease, the Mongolian gerbil, to examine the effects of the extract on both prevention and eradication of infection. The extract was administered to Mongolian gerbils at a daily dose of 100 mg/kg body weight in rations either 3 weeks prior to infection or 6 weeks post-infection. Treatment with the standardized ginger extract reduced H. pylori load as compared with controls and significantly (P<0.05) reduced both acute and chronic muscosal and submucosal inflammation, cryptitis, as well as epithelial cell degeneration and erosion induced by H. pylori. Importantly, the extract did not increase morbidity or mortality. Further investigations of the mechanism demonstrated that the ginger extract inhibited the activity of cyclooxygenase-2, with 50% inhibitory concentration (IC(50)) of 8.5 mug/mL in vitro, inhibited the nuclear factor-kappaB transcriptional response in kBZ Jurkat cells (human T lymphocytes) with an IC(50) of 24.6 mug/mL, and significantly inhibited the release of interleukin (IL)-1beta, IL-6, IL-8, and tumor necrosis factor-alpha from lipopolysaccharide-stimulated human peripheral blood mononuclear cells with IC(50) values of 3.89, 7.7, 8.5, and 8.37 mug/mL, respectively. These results suggest ginger extracts may be useful for development as agents to reduce H. pylori-induced inflammation and as for gastric cancer chemoprevention.

Figure 1

Structures of the gingerols and shogoal from ginger rhizome extract.

Figure 2

Outline of prevention and treatment studies in Mongolian gerbils infected with Helicobacter pylori (Hp) strain B128. In the prevention study, treatment chow was started 3 weeks prior to infection and lasted a total of 9 weeks prior to sacrifice (Sac). In the treatment study, treatment was started 6 weeks post-infection and lasted for 4 weeks, with a return to normal chow for 4 weeks following treatment, prior to sacrifice.