硫糖铝对胃黏膜钙通道活性的影响。

Effect of sucralfate on gastric mucosal calcium channels activity.

Liu J, Slomiany A, Slomiany B L

Research Center, New Jersey Dental School, University of Medicine and Dentistry of New Jersey, Newark 07103.

Gen Pharmacol. 1992 Nov;23(6):1129-33. doi: 10.1016/0306-3623(92)90299-y.

Abstract

The effect of anti-ulcer agent, sucralfate, on the activity of the gastric mucosal calcium channel was investigated using calcium channels purified from rat gastric epithelial cell membranes. 2. The channels on reconstitution into phosphatidylcholine vesicles responded in a concentration-dependent manner to a calcium channel activator, BAY K8644, as well as to a calcium channel antagonist, PN200-110. The 45Ca2+ uptake was inhibited by sucralfate. Maximum inhibitory effect was attained at 100 micrograms/ml sucralfate, at which point a 52% decrease in the uptake occurred. 3. EGF-induced channel protein phosphorylation showed an increase in tyrosine phosphorylation of 55 and 170 kDa proteins, and the vesicles containing the phosphorylated channels displayed a 48% greater 45Ca2+ uptake. This phosphorylation process was inhibited by sucralfate. Furthermore, sucralfate also interfered with the binding of EGF to calcium channel protein. 4. The results indicate that sucralfate protects the cellular integrity from calcium imbalance by modulating the EGF-stimulated gastric mucosal calcium channel phosphorylation.

摘要

使用从大鼠胃上皮细胞膜纯化的钙通道，研究了抗溃疡药物硫糖铝对胃黏膜钙通道活性的影响。2. 重组到磷脂酰胆碱囊泡中的通道对钙通道激活剂BAY K8644以及钙通道拮抗剂PN200 - 110呈浓度依赖性反应。硫糖铝抑制了45Ca2+摄取。在硫糖铝浓度为100微克/毫升时达到最大抑制效果，此时摄取量下降了52%。3. 表皮生长因子（EGF）诱导的通道蛋白磷酸化显示55和170 kDa蛋白的酪氨酸磷酸化增加，含有磷酸化通道的囊泡显示45Ca2+摄取增加48%。该磷酸化过程被硫糖铝抑制。此外，硫糖铝还干扰了EGF与钙通道蛋白的结合。4. 结果表明，硫糖铝通过调节EGF刺激的胃黏膜钙通道磷酸化来保护细胞完整性免受钙失衡的影响。