Beil W, Birkholz C, Wagner S, Sewing K F
Department of General Pharmacology, Hannover Medical School, Germany.
Prostaglandins Leukot Essent Fatty Acids. 1998 Aug;59(2):119-25. doi: 10.1016/s0952-3278(98)90090-4.
The effect of the Helicobacter pylori (H. pylori) fatty acid cis 9,10-methyleneoctadecanoic acid (MOA) on gastric acid secretion was studied in isolated guinea-pig parietal cells. MOA (1 and 3 micromol/l) stimulated basal and enhanced histamine- and dibutyryl cyclic AMP-stimulated acid secretion in parietal cells. MOA increased intracellular free [Ca2+]i concentration in a concentration-dependent manner. The source of [Ca2+]i was extracellular as demonstrated by depletion of [Ca2+]i with EGTA. Furthermore, MOA caused activation of parietal cell protein kinase C (PKC). The effect of MOA upon PKC activation was [Ca2+]i-dependent but did not require phosphatidylserine as phospholipid co-factor. Similarly to the effect of diolein, MOA increased the stimulatory effect of phosphatidylserine at low [Ca2+]i concentrations. Treatment of parietal cells with MOA caused translocation of PKC from the cytosol to the membrane-associated cell fraction. We propose that MOA stimulates parietal cell acid secretion presumably by an increase of cytosolic free [Ca2+]i concentrations and PKC activation.
在分离的豚鼠壁细胞中研究了幽门螺杆菌（H. pylori）脂肪酸顺式9,10-亚甲基十八烷酸（MOA）对胃酸分泌的影响。MOA（1和3微摩尔/升）刺激壁细胞的基础胃酸分泌，并增强组胺和二丁酰环磷酸腺苷刺激的胃酸分泌。MOA以浓度依赖性方式增加细胞内游离[Ca2+]i浓度。如用EGTA耗尽[Ca2+]i所证明，[Ca2+]i的来源是细胞外的。此外，MOA导致壁细胞蛋白激酶C（PKC）活化。MOA对PKC活化的作用是[Ca2+]i依赖性的，但不需要磷脂酰丝氨酸作为磷脂辅因子。与二油精的作用类似，在低[Ca2+]i浓度下，MOA增加了磷脂酰丝氨酸的刺激作用。用MOA处理壁细胞导致PKC从胞质溶胶转位至膜相关细胞部分。我们提出，MOA可能通过增加胞质游离[Ca2+]i浓度和PKC活化来刺激壁细胞胃酸分泌。
