【摘要】 目的:课题组整体外周血研究提示粒细胞-巨噬细胞集落刺激因子(GM-CSF)、活化正常T细胞表达分泌调节物(RANTES)与脾胃湿热证相关;从局部胃黏膜进一步探讨其在幽门螺杆菌(Hp)相关胃病脾胃湿热证发病中的作用。方法:收集胃黏膜标本114份(包括慢性胃炎68例、消化性溃疡34例;脾胃湿热证83例、脾气虚证19例;健康受试者12名);以快速尿素酶和美兰染色进行Hp检测;HE染色评定炎性反应程度及活动度;Elivision plus定性定位检测GM-CSF、RANTES蛋白表达。结果:脾胃湿热证胃黏膜Hp感染率和程度以及炎性反应程度、活动性均较脾气虚证明显。Hp感染脾胃湿热、脾气虚证胃黏膜炎性反应程度及活动程度显著高于非感染者(P<0.05)。Hp感染脾胃湿热证炎性活动度重于脾气虚证,差异具有显著性(P<0.05);且胃黏膜萎缩、肠上皮化生病理改变有较脾气虚证明显的趋势。GM-CSF、RANTES蛋白表达定位于胃黏膜上皮和腺体胞浆,Hp感染尤其脾胃湿热证高于非感染者。结论:Hp可能作为引发或加重脾胃湿热证的重要原因,其促使GM-CSF和RANTE表达并参与脾胃湿热"邪正交争"的亢奋状态,引起更为严重的炎性反应及活动性程度,并可能促使胃黏膜形成萎缩及肠上皮化生的病理改变,或许这正是Hp相关胃病炎性病理改变以脾胃湿热证更为严重的原因之一。更多还原

【Abstract】 Objective: Study before has indicated that expression of GM-CSF, RANTES in peripheral blood of human was related to spleen and stomach dampness-heat syndrome(DHS); this study further explores its role in DHS of Hp related gastropathy via immunohistochemical staining in gastric mucosa. Methods: A total of 114 specimens of gastric mucosa in this study were recruited [including 68 cases chronic gastritis, 34 cases peptic ulcer; 83 cases DHS, 19 cases deficiency of spleen qi syndrome(PDS); 12 healthy subjects]; Hp infection was indicated with rapid urease and methylene blue testing; Degree and activity of inflammation were investigated by hematein eosin; Elivision plus qualitative and positioning of GM-CSF and RANTES were performed. Results: Proportion and degree of Hp infection, degree and activity of inflammation in DHS gastric mucosa were higher than PDS. Hp infected individual showed a significantly severer inflammation degree and activity than Hp negative individual in DHS and PDS groups(P<0.05). Inflammation activity in DHS with Hp infected is more serious than PDS(P<0.05); there is a similar tendency in these two group in intestinal metaplasia and hyperplasia pathological changes. GM-CSF and RANTES expressed at epithelium and glands cytoplasm of gastric mucosa. Also, these proteins displayed higher expression in Hp positive individual compared with Hp negative. Conclusion: Hp may act as one of factors that induces or promotes DHS development which leads to expression of GM-CSF and RANTE, then makes a contribution to intense struggle between vital qi and pathogenic qi in DHS. This results in severer inflammation as well as activity significantly and seems to induce atrophy and intestinal metaplasia. It probably could account for serious pathologic change in Hp-related gastric disease.更多还原