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目的 研究果胶铋对胃粘膜损伤的保护机制 ,探讨胃粘膜细胞中三叶肽因子 2信使核糖核酸 (TFF2 mRNA)表达及前列腺素E2 (PGE2 )在果胶铋胃粘膜保护机制中的作用。方法 建立阿斯匹林胃粘膜损伤模型 ,细胞原位杂交结合图像分析检测TFF2 mRNA表达水平并以阳性细胞平均光度值 (OD)表示 ,放射免疫法测胃粘膜PGE2 浓度 ,Guth法计算胃粘膜损伤指数。结果 果胶铋组与未用药组TFF2 mRNA的OD值分别为 0 .5 6± 0 .0 9、0 .2 8± 0 .0 4,PGE2 浓度分别为 (4.2 0± 0 .85 )Hg/ml、(1.18± 0 .14)Hg/ml,果胶铋组高于未用药组 ,二项结果相比均有显著性差异 (P <0 .0 5 ) ;果胶铋组损伤指数为(8.6 0± 2 .2 0 )极明显低于未用药组 (2 9.72± 6 .5 3) ,P <0 .0 1;经相关分析 ,果胶铋组胃粘膜细胞TFF2 mRNA的表达水平增加与胃粘膜PGE2 浓度增加无相关性 (r=0 .48,P >0 .0 5 )。结论 果胶铋对阿斯匹林引起的胃粘膜损伤有显著的保护作用 ,可能与其增加TFF2 mRNA的表达及促进胃粘膜PGE2 合成有关
Objective To investigate the protective mechanism of bismuth pectate against gastric mucosal lesion, and to explore the role of TFF2 mRNA expression in gastric mucosal cells and the protective effect of prostaglandin E2 (PGE2) on the gastric mucosal protective mechanism of pectin bismuth. Methods The gastric mucosal lesion model of aspirin was established. The expression of TFF2 mRNA was detected by in situ hybridization and image analysis. The expression of PGF2 was detected by radioimmunoassay. The gastric mucosal damage was calculated by Guth method index. Results The OD values of TFF2 mRNA in pectin group and non-treated group were 0.56 ± 0.09,0.28 ± 0.4 and PGE2 concentrations were (4.2 ± 0.85) Hg / ml, (1.18 ± 0.14) Hg / ml, pectin bismuth group was higher than the non-medication group, the two results were significantly different (P <0.05); pectin bismuth group injury index 8.6 ± 2.20) was significantly lower than that of the untreated group (2 9.72 ± 6.53), P <0.01; the correlation analysis showed that the expression level of TFF2 mRNA in gastric mucosal cells increased Gastric mucosa increased PGE2 concentration was not related (r = 0.48, P> 0.05). Conclusion Pectin bismuth has a significant protective effect on gastric mucosal damage induced by aspirin, which may be related to the increase of TFF2 mRNA expression and the promotion of gastric mucosal PGE2 synthesis