Oxygen metabolites modulate prostaglandin E2 production by isolated gastric mucosal cells.
Oxygen metabolites modulate prostaglandin E2 production by isolated gastric mucosal cells.
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氧代谢物调节分离的胃粘膜细胞产生前列腺素 E2。
DOI：
10.1152/ajpgi.1989.256.5.g925
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发表时间：
1989
期刊：
影响因子：
--
通讯作者：
Soll,AH
中科院分区：
文献类型：
--
作者：
Olson,CE;Chen,MC;Amirian,DA;Soll,AH
我们先前发现，犬胃粘膜分离细胞中的一小部分是前列腺素E2(PGE2)的主要产生细胞，并确定巨噬细胞是主要的细胞来源。前列腺素H合成酶的活性依赖于过氧化氢的持续存在。由于活性氧代谢产物可能介导炎症或缺血性疾病中的粘膜损伤，我们研究了分离的胃细胞在暴露于氧代谢产物生成系统黄嘌呤和黄嘌呤氧化酶时PGE2的释放。我们发现在不裂解细胞的情况下，黄嘌呤氧化酶浓度和PGE2产量之间存在浓度依赖关系。氧化剂刺激的最大PGE2产量相当于PGE2对缓激肽和A23187的最大反应。头细胞部分和顶层细胞部分产生的前列腺素E_2非常少，黄嘌呤氧化酶的浓度可以刺激小细胞部分产生最大的前列腺素E_2。尿酸不能刺激PGE2的产生。过氧化氢酶完全抑制该反应，而超氧化物歧化酶有部分抑制作用。过氧化氢刺激浓度依赖的前列腺素E_2的产生，其ED50约为5微米。我们的结论是，活性氧代谢产物通过胃粘膜的小细胞部分刺激PGE2的产生。
We previously found that the small cell fraction of isolated cells from canine gastric mucosa is a major producer of prostaglandin E2 (PGE2) and identified macrophages as the predominant cellular source. Prostaglandin-H synthase activity is dependent on the continuous presence of hydroperoxides. Because reactive oxygen metabolites may mediate mucosal injury in inflammatory or ischemic disease, we studied the release of PGE2 by isolated gastric cells during exposure to an oxygen metabolite-generating system, xanthine and xanthine oxidase. We found a concentration-dependent relationship between xanthine oxidase concentration and PGE2 production without cell lysis. The maximum PGE2 production stimulated by oxidants was equivalent to the maximum PGE2 response to bradykinin and A23187. The chief and parietal cell fractions produced very little PGE2 with xanthine oxidase concentrations that stimulated maximal PGE2 production in the small cell fraction. Uric acid did not stimulate PGE2 production. Catalase completely inhibited the response, while superoxide dismutase had a partial inhibitory effect. Hydrogen peroxide stimulated concentration-dependent PGE2 production with an ED50 of approximately 5 microM. We concluded that reactive oxygen metabolites stimulate PGE2 production by the small cell fraction of gastric mucosa.