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Background   Kaempferia parviflora  (KP) has been used in traditional Thai medicine to cure gastrointestinal disorders since ancient times.  Helicobacter pylori  is an initiating factor in gastric pathogenesis via activation of massive inflammation, the cumulative effect of which leads to gastric disease progression, including gastric carcinogenesis. Accordingly, the effect of a crude ethyl acetate extract of KP (CEAE-KP) on proinflammatory cytokine production and cell chemotaxis was the focus of this study.    Methods  The cytotoxicity of CEAE-KP (8–128 μg/ml) on AGS (gastric adenocarcinoma) cells was determined at 6, 12 and 24 h using an MTT assay. The effect of CEAE-KP on  H. pylori -induced interleukin (IL)-8 production by AGS cells was evaluated by ELISA and RT-PCR. The effect of CEAE-KP on monocyte and neutrophil chemotaxis to  H. pylori  soluble protein (sHP) and IL-8, respectively, was determined using a Boyden chamber assay with THP-1 or HL-60 cells.    Results  CEAE-KP reduced AGS cell viability in a concentration- and time-dependent manner, but at 8–16 μg/ml, it was not cytotoxic after 6–24 h of exposure. Coculture of AGS cells with CEAE-KP at a noncytotoxic concentration of 16 μg/ml and  H. pylori  reduced IL-8 secretion by ~ 60% at 12 h, which was consistent with the decreased level of mRNA expression, and inhibited neutrophil chemotaxis to IL-8. sHP (100 ng/ml) induced marked monocyte chemoattraction, and this was decreased by ~ 60% by CEAE-KP.    Conclusion  CEAE-KP might serve as a potent alternative medicine to ameliorate the inflammation mediated by  H. pylori  infection.

bmc complementary medicine and therapies

Ethyl acetate extract of Kaempferia parviflora inhibits Helicobacter pylori-associated mammalian cell inflammation by regulating proinflammatory cytokine expression and leukocyte chemotaxis