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目的 :探讨一氧化氮 (NO)、内皮素 (ET- 1)、表皮生长因子受体 (EGFR)在乙酸性慢性胃溃疡大鼠中的作用及相互关系。方法 :采用乙酸性慢性胃溃疡疾病模型 ,游标卡尺测定溃疡指数 ,硝酸还原酶法测定 NO含量 ,放射免疫法检测血浆 ET- 1含量 ,SABC免疫组织化学方法及图像分析观察 EGFR在溃疡周围粘膜的表达。结果 :左旋精氨酸 (L - Arg)组溃疡指数与模型组及亚硝基左旋精氨酸 (L - NNA )组比较显差有显著性意义 (P <0 .0 5 ,<0 .0 1) ;L- Arg组血清 NO及血浆 ET- 1含量与对照组、模型组及 L- NNA组比较差异有显著性意义 (P <0 .0 5 ,<0 .0 1) ;L - NNA组血清 NO及血浆 ET- 1含量与模型组及对照组比较差异均有非常显著性意义 (均 P <0 .0 1) ;L -Arg组 EGFR表达较模型组、L- NNA组及对照组显著增加 (积分光密度值及阳性细胞占总面积百分比均 P <0 .0 5 ) ;L- NNA组 EGFR显著弱于模型组 (P<0 .0 1)。结论 :NO前体 L- Arg可以诱导、促进 NO合成 ,反馈性地抑制 ET- 1的释放 ,从而维持 NO和 ET的动态平衡及胃粘膜 EGFR正常水平表达 ,促进溃疡愈合。
Objective: To investigate the role and relationship of nitric oxide (NO), endothelin (ET-1) and epidermal growth factor receptor (EGFR) in rats with chronic acetic acid-induced gastric ulcer. Methods: The model of chronic gastric ulcer caused by acetic acid was used. The ulcer index was determined by vernier caliper, the content of NO was measured by nitrate reductase method. The content of plasma ET-1 was detected by radioimmunoassay. The expression of EGFR in mucosa around the ulcer was observed by SABC immunohistochemistry and image analysis . Results: The ulcer index of L - Arg group was significantly lower than that of model group and L - NNA group (P <0.05, <0. 0 1). There was significant difference of serum NO and ET-1 levels between L-Arg group and control group, model group and L-NNA group (P <0.05, <0.01) Compared with the model group and the control group, serum NO and ET-1 levels were significantly different (all P <0.01); EGFR expression in L-Arg group was significantly higher than that in model group, L-NNA group and control group (P <0.05). The EGFR of L-NNA group was significantly weaker than that of model group (P <0.01). CONCLUSION: L-Arg, a NO precursor, can induce and promote the synthesis of NO and inhibit ET-1 release retrospectively, thus maintaining the homeostasis of NO and ET and the normal expression of EGFR in gastric mucosa and promoting the healing of ulcer.