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目的 探讨表皮生长因子 (EGF)对大鼠慢性萎缩性胃炎 (CAG)胃黏膜病变的作用。方法 将已经建立的SD大鼠CAG模型随机分成治疗组和对照组 ,治疗组给予EGF 10 μg/kg皮下注射 ,每日 1次 ;对照组给予等容生理盐水皮下注射 ,每日 1次 ,刺激 12周后取出全胃 ,观察各组大鼠胃黏膜病理变化。结果 治疗组大鼠胃黏膜炎性细胞浸润程度较对照组明显减轻 (P <0 0 1) ;两组大鼠胃黏膜腺体层厚度分别为 (2 15 0± 2 0 7) μm和 (139 2± 13 8) μm(P <0 0 1) ,胃黏膜腺体层厚度 /黏膜肌层厚度分别为 2 70± 0 34和 1 2 7± 0 2 7(P <0 0 1) ,单位长度内胃黏膜腺体数目分别为 2 6 2 0± 1 2 7和 19 90± 1 78(P <0 0 1) ;治疗组胃黏膜腺体增殖细胞核抗原 (PCNA)表达阳性的宽度 (77 70± 4 16 ) μm较对照组 (5 4 40± 4 5 4) μm明显增加 (P <0 0 1)。治疗组大鼠胃黏膜腺体排列规则 ,未发现有恶性增殖现象。结论 EGF对SD大鼠CAG模型的胃黏膜萎缩有逆转治疗作用。EGF促进大鼠胃黏膜细胞PCNA阳性表达是其对大鼠CAG损伤的保护性增殖作用
Objective To investigate the effect of epidermal growth factor (EGF) on gastric mucosal lesions in rats with chronic atrophic gastritis (CAG). Methods The established CAG model of SD rats was randomly divided into treatment group and control group. The treatment group was injected subcutaneously with EGF 10 μg / kg once a day. The control group was given isocratical normal saline subcutaneously once a day After 12 weeks, the whole stomach was taken out and the pathological changes of gastric mucosa in each group were observed. Results The infiltration of inflammatory cells in gastric mucosa in treatment group was significantly lower than that in control group (P <0.01). The gastric mucosal glandular layer thicknesses were (2 15 0 ± 2 0 7) μm and (139 2 ± 13 8) μm (P <0.01). The thickness of gastric mucosa glandular layer / mucosa muscular layer were 2 70 ± 0 34 and 122 7 ± 0 2 7, respectively The numbers of gastric mucosal glands in the treatment group were respectively 2620 ± 1 27 and 19 90 ± 1 78 (P <0.01), and the positive expression of proliferating cell nuclear antigen (PCNA) in the gastric mucosa was 77 70 ± 4 16 μm was significantly higher than that of the control group (5 4 40 ± 4 5 4) μm (P 0 01). The treatment group gastric mucosal glands arranged rules, no malignant proliferation was found. Conclusion EGF can reverse the gastric mucosal atrophy in the CAG model of SD rats. The positive expression of PCNA induced by EGF in rat gastric mucosal cells is a protective proliferative effect on CAG injury in rats