Arakawa T, Fukuda T, Kobayashi K, Kobayashi K, Tarnawski A
Third Department of Internal Medicine, Osaka City University Medical School, Japan.
Digestion. 1996;57(1):41-6. doi: 10.1159/000201311.
Prostaglandins reduce damage by noxious agents to isolated gastric cells. The mechanism remains unexplained. This study was done to examine involvement of microtubules with prostaglandin-mediated cell protection. Cultured mucus-producing cells of rat gastric mucosa were used. Cultured cells were incubated with 16, 16-dimethyl-prostaglandin E2 (dmPGE2), colchicine, or vehicle alone in calcium-containing (1.3 mM) and calcium-free medium. The cells were then exposed to 8% ethanol. Cell integrity and damage were assessed by 51Cr release and in part by transmission electron microscopy (TEM). Specific 51Cr release was closely related to percentage change of necrotic cells assess by TEM. Cell damage caused by 8% ethanol was greater in medium-containing calcium than in calcium-free medium. dmPGE2 at 10(-5) M inhibited cell damage in calcium-containing medium. Colchicine itself at concentrations up to 10(-5) M did not affect cell integrity, but at 10(-5) M concentration potentiated damage caused by 8% ethanol in calcium-containing medium. Pretreatment with 10(-5) M colchicine abolished the protective effect of dmPGE2. Microtubules may mediate protection by dmPGE2 of cultured gastric cells against ethanol damage.
前列腺素可减少有害因子对离体胃细胞的损伤。其机制尚不清楚。本研究旨在探讨微管在前列腺素介导的细胞保护中的作用。使用大鼠胃黏膜培养的黏液分泌细胞。将培养的细胞分别与16,16 - 二甲基前列腺素E2（dmPGE2）、秋水仙碱或单独的溶剂在含钙（1.3 mM）和无钙培养基中孵育。然后将细胞暴露于8%乙醇中。通过51Cr释放评估细胞完整性和损伤，部分通过透射电子显微镜（TEM）评估。特异性51Cr释放与通过TEM评估的坏死细胞百分比变化密切相关。8%乙醇引起的细胞损伤在含钙培养基中比在无钙培养基中更大。10(-5) M的dmPGE2可抑制含钙培养基中的细胞损伤。秋水仙碱本身在浓度高达10(-5) M时不影响细胞完整性，但在10(-5) M浓度时可增强8%乙醇在含钙培养基中引起的损伤。用10(-5) M秋水仙碱预处理可消除dmPGE2的保护作用。微管可能介导dmPGE2对培养的胃细胞免受乙醇损伤的保护作用。
