Helicobacter pylori is now recognized as an important cause of type B gastritis, which is strongly associated with gastric and
duodenal ulcer disease. H. pylori may be a causative factor in patients with gastric cancer. The growth inhibition and N-acetylation
of 2-Aminofluorene (AF) or P-aminobenzoic acid (PABA) by arylamine N-acetyltransferase (NAT) in H. pylori were inhibited by
luteolin, a component in herbal medicine. The growth inhibition was based on the changes of optical density (OD) by using a
spectrophotometer. The N-acetylation of AF or PABA by NAT from H. pylori were assayed by the amounts of acetylated and nonacetylated
AF or PABA in cytsols and intact bacteria of H. pylori by using HPLC. An inhibition of growth on H. pylori demonstrated
that luteolin elicited a dose-dependent growth inhibition in the H. pylori cultures. Cytosols and suspensions of H. pylori with
or without specific concentrations of luteolin co-treatment showed different percentages of AF or PABA acetylation. The data
indicated that there was decreased NAT activity associated with increased levels of luteolin in H. pylori cytosols and suspensions.
Using standard steady-state kinetic analysis, it was demonstrated that luteolin was a possible uncompetitive inhibitor to NAT
enzyme in H. pylori. This report is the first demonstration to show that luteolin can inhibit H. pylori growth and NAT activity.
