Effects of prostaglandins on gastrin release from canine antral mucosal cells in primary culture.
Effects of prostaglandins on gastrin release from canine antral mucosal cells in primary culture.
复制标题
前列腺素对原代培养物中犬胃窦粘膜细胞胃泌素释放的影响。
DOI：
10.1152/ajpgi.1994.266.2.g194
复制
发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Soll,AH
中科院分区：
文献类型：
--
作者：
Schepp,W;Chan,CB;Giraud,AS;Avedian,D;Chen,MC;Chew,P;Walsh,JH;Soll,AH
体内研究表明内源性和外源性的胰高血糖素可以改变胃泌素的分泌。我们已经使用了原代培养物含有犬胃窦G细胞研究细胞的作用，对胃泌素分泌，比较前列腺素E2（PGE 2）和它的合成类似物恩前列素的影响。恩前列素（10（-10）-10（-6）M）抑制蛙皮素、卡巴胆碱和毛喉素（后者是腺苷酸环化酶的受体非依赖性激活剂）引起的胃泌素分泌。用百日咳毒素（200 ng/ml，8 h）处理可逆转恩前列素的这种抑制作用。然而，恩前列素不抑制受体后刺激8-溴腺苷3 '，5'-环一磷酸（10（-3）M）、钙离子载体A-23187（10（-7）M）或4 β-佛波醇12-肉豆蔻酸酯13-乙酸酯（10（-8）M）。相比之下，而PGE 2抑制毛喉素刺激的胃泌素释放，PGE 2不抑制卡巴胆碱或蛙皮素在对照培养物的反应。然而，在百日咳毒素处理的文化，PGE 2抑制被逆转，相反，铃蟾肽，卡巴胆碱，并可能毛喉素的反应增强。吲哚美辛在10（-5）M的剂量没有改变基础或铃蟾肽刺激的胃泌素分泌。然而，生长抑素抗体CURE-S6增强了对毛喉素的反应，并增强了PGE 2的抑制作用，这表明内源性生长抑素在这些培养物中产生了抑制性音调，并排除了PGE 2通过释放内源性生长抑素发挥作用的可能性。我们的数据表明，在培养的胃窦细胞胃泌素的释放是由抑制和刺激前列腺素机制。（250字处删节）
Evidence in vivo indicates that endogenous and exogenous prostaglandins can alter gastrin secretion. We have used primary cultures containing canine antral G-cells to study the cellular actions of prostaglandins on gastrin secretion, comparing the effects of prostaglandin E2 (PGE2) and its synthetic analogue enprostil. Enprostil (10(-10)-10(-6) M) inhibited gastrin secretion in response to bombesin, carbachol, and forskolin, the latter a receptor-independent activator of adenylate cyclase. This inhibition by enprostil was reversed by treatment with pertussis toxin (200 ng/ml, 8 h). However, enprostil did not inhibit the postreceptor stimuli 8-bromoadenosine 3',5'-cyclic monophosphate (10(-3) M), calcium ionophore A-23187 (10(-7) M), or 4 beta-phorbol 12-myristate 13-acetate (10(-8) M). In contrast, whereas PGE2 inhibited forskolin-stimulated gastrin release, PGE2 did not inhibit the response to carbachol or bombesin in control cultures. However, in pertussis toxin-treated cultures, PGE2 inhibition was reversed and, in contrast, the responses to bombesin, carbachol, and possibly forskolin were augmented. Indomethacin at a dose of 10(-5) M did not alter basal or bombesin-stimulated gastrin secretion. However, the somatostatin antibody CURE-S6 enhanced the response to forskolin and enhanced inhibition by PGE2, suggesting that endogenous somatostatin produced an inhibitory tone in these cultures and excluding the possibility that PGE2 acted via release of endogenous somatostatin. Our data suggest that in cultured antral cells gastrin release is regulated by inhibitory and stimulatory prostaglandin mechanisms.(ABSTRACT TRUNCATED AT 250 WORDS)