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目的 通过幽门螺杆菌（Ｈｐ） 的脂多糖抗原对体外大鼠肠嗜铬样细胞功能的影响，深入探讨Ｈｐ 改变胃酸分泌和黏膜增生的病理机制。方法 通过链球蛋白酶消化、淘析法和梯度离心分离出纯化率９５％ 、成活率＞ ９０ ％ 的大鼠胃的肠嗜铬样细胞。短期培养后通过酶标免疫法，ＢｒｄＵ掺入试验分别测定肠嗜铬样细胞基础和刺激后的组胺分泌及ＤＮＡ 增生。结果 脂多糖抗原刺激基础组胺的分泌（ＥＣ５０４ ×１０－１１ ｍｏｌ／Ｌ） ，同时显著增强胃泌素刺激组胺分泌的作用（ＥＣ５０ １０－１０ ｍｏｌ／Ｌ）。生长抑素（１０－１２ ｍｏｌ／Ｌ）能完全抑制这些作用而胃泌素拮抗剂Ｌ３６５２６０ 则无明显抑制作用。脂多糖抗原不能刺激肠嗜铬样细胞的ＤＮＡ合成，但明显增强胃泌素对其ＤＮＡ的合成（ＥＣ５０ １０－１０ ｍｏｌ／Ｌ）。大肠杆菌的脂多糖抗原（１０－ １２ ～１０ －６ ｍｏｌ／Ｌ） 对肠嗜铬样细胞的组胺分泌和ＤＮＡ合成均无明显作用。结论 在体外，Ｈｐ 直接影响肠嗜铬样细胞的增生和分泌。高度提示脂多糖抗原同肠嗜铬样细胞的互相作用参于了Ｈｐ 感染引起的酸分泌异常和胃黏膜的病理改变。
Objective To investigate the effect of Hp on the function of enterochromaffin-like cells in vitro and to explore the pathological mechanism of Hp changing gastric acid secretion and mucosal hyperplasia. Methods Gastric chromaffin-like cells of rat stomach were isolated by streptavidin digestion, elutriation and gradient centrifugation. The purification rate was 95% and the survival rate was> 90%. Short-term culture by enzyme-linked immunosorbent assay, BrdU incorporation assay determination of enterochromaffin-like cells based on stimulation and histamine secretion and DNA proliferation. Results The lipopolysaccharide antigen stimulated the secretion of basal histamine (EC504 × 10-11 mol / L) and markedly enhanced the effect of gastrin-stimulated histamine secretion (EC50 10-10 mol / L). Somatostatin (10-12 mol / L) can completely inhibit these effects and gastrin antagonist L365260 has no significant inhibitory effect. Lipopolysaccharide antigen can not stimulate the DNA synthesis of enterochromaffin-like cells, but significantly enhance the synthesis of gastrin (EC50 10-10 mol / L). Escherichia coli lipopolysaccharide antigen (10-12 ~ 10 -6 mol / L) had no significant effect on histamine secretion and DNA synthesis of enterochromaffin-like cells. Conclusion In vitro, Hp directly affects the proliferation and secretion of enterochromaffin-like cells. It is highly suggestive that the interaction of lipopolysaccharide antigen with enterochromaffin-like cells takes part in the abnormal acid secretion caused by Hp infection and the pathological changes of gastric mucosa.