Konda Y, Nishisaki H, Nakano O, Matsuda K, Wada K, Matozaki T, Nagao M, Sakamoto C
Second Department of Internal Medicine, Kobe University School of Medicine, Japan.
Nihon Shokakibyo Gakkai Zasshi. 1991 Jun;88(6):1281-7.
The mechanism by which PGE2 directly protects individual gastric cells from ethanol-induced injury was studied by using isolated gastric chief cells from guinea pig. Ethanol dose-dependently caused chief cell injury which was estimated by the release of lactate dehydrogenase (LDH) from chief cells. Pretreatment of chief cells with PGE2 reduced the cell damage caused by ethanol in time- and dose-dependent manner. The pretreatment at 37 degrees C and pH 7.4 with PGE2 maximally reduced the cell damage. This protective effect was reduced when the pretreatment was performed at either acid or alkaline pH or at reduced temperature. PGE2 did not stimulate any increase in cytosolic free Ca2+ concentration and initial Ca2+ influx rate. On the other hand, PGE2 stimulated an increase of cAMP accumulation in chief cells. However, pretreatment of chief cells with secretion, VIP, dbcAMP or forskolin failed to reduce subsequent injury caused by ethanol. These results suggest that PGE2 may protect chief cells against ethanol-caused injury probably via PGE type receptors coupled to as yet unidentified signal in gastric chief cells.
通过使用豚鼠分离的胃主细胞,研究了PGE2直接保护单个胃细胞免受乙醇诱导损伤的机制。乙醇以剂量依赖性方式导致主细胞损伤,这通过主细胞中乳酸脱氢酶(LDH)的释放来评估。用PGE2预处理主细胞可及时且剂量依赖性地减少乙醇引起的细胞损伤。在37℃和pH 7.4下用PGE2预处理可最大程度地减少细胞损伤。当在酸性或碱性pH或降低的温度下进行预处理时,这种保护作用会降低。PGE2不会刺激细胞质游离Ca2+浓度和初始Ca2+内流速率的任何增加。另一方面,PGE2刺激主细胞中cAMP积累增加。然而,用分泌素、VIP、dbcAMP或福斯可林预处理主细胞未能减少随后由乙醇引起的损伤。这些结果表明,PGE2可能通过与胃主细胞中尚未确定的信号偶联的PGE型受体保护主细胞免受乙醇引起的损伤。