Beil W, Birkholz C, Sewing K F
Institut für Allgemeine Pharmakologie, Medizinische Hochschule Hannover, Germany.
Arzneimittelforschung. 1995 Jun;45(6):697-700.
The effect of the flavonoids flavone, flavanone and quercetin on parietal cell acid production, H+/K(+)-ATPase activity, gastric mucosal prostaglandin E2 biosynthesis and Helicobacter pylori growth was studied. All flavonoids inhibited acid production in isolated parietal cells in response to histamine and dibutyryl-cAMP stimulation (IC50 values between 26 and 139 mumol/l) and inhibited H+/K(+)-ATPase activity. Inhibition of H+/K(+)-ATPase activity was dependent on the ATP concentration. Fluorescence measurements showed that flavanone reacts with ATP. These findings indicate that the inhibitory action of flavonoids on H+/K(+)-ATPase activity is related to their ability to complex ATP. Flavone and flavanone (10 and 100 mumol/l) stimulated prostaglandin E2 production in isolated gastric mucosal cells. Furthermore, the compounds inhibited Helicobacter pylori growth in a concentration-dependent manner. From these finding it appears that flavonoids are a group of compounds which could have a therapeutic potential for treatment of gastrointestinal diseases associated with Helicobacter pylori infection.
研究了黄酮、黄烷酮和槲皮素这几种黄酮类化合物对壁细胞产酸、H⁺/K⁺-ATP酶活性、胃黏膜前列腺素E2生物合成以及幽门螺杆菌生长的影响。所有黄酮类化合物均能抑制组胺和二丁酰环磷腺苷刺激下分离的壁细胞产酸（IC50值在26至139μmol/L之间），并抑制H⁺/K⁺-ATP酶活性。H⁺/K⁺-ATP酶活性的抑制作用取决于ATP浓度。荧光测量表明黄烷酮与ATP发生反应。这些发现表明黄酮类化合物对H⁺/K⁺-ATP酶活性的抑制作用与其络合ATP的能力有关。黄酮和黄烷酮（10和100μmol/L）可刺激分离的胃黏膜细胞中前列腺素E2的产生。此外，这些化合物以浓度依赖的方式抑制幽门螺杆菌的生长。从这些发现来看，黄酮类化合物似乎是一类对治疗与幽门螺杆菌感染相关的胃肠道疾病具有治疗潜力的化合物。
