表皮生长因子对慢性萎缩性胃炎大鼠胃黏膜病理变化的影响

Jiaguo Wu, J. Si, Q. Cao, Wen Lu, Jian Wang, Bingjian Lu, N. Dai
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摘要

目的:研究表皮生长因子(EGF)对慢性萎缩性胃炎(CAG)大鼠胃黏膜病理变化的影响。方法:将建立的CAG大鼠模型分为A、b组,A组大鼠皮下注射EGF 10 μg/kg;B组大鼠皮下注射等量生理盐水。12周后,用颈椎脱位法处死大鼠,镜检胃黏膜。结果:A组炎症细胞浸润分级低于B组(P < 0.01)。胃粘膜腺层厚度A组为215.0±20.7 μm, B组为139.2±13.8 μm (P < 0.01)。胃粘膜腺厚度与肌层厚度之比(L1/L2) A组为2.70±0.34,B组为1.27±0.27 (P < 0.01)。在1 mm长度的粘膜层中,a组的胃腺数为26.20±1.27个,B组的胃腺数为19.90±1.78个(P < 0.01)。A组胃腺重排,无恶性增生征象。表达增殖细胞核抗原(PCNA)的胃粘膜宽度A组大于B组(77.70±4.16 μm vs 54.40±4.54 μm);P < 0.01)。结论:表皮生长因子在逆转CAG大鼠胃粘膜萎缩中具有治疗作用。促进PCNA的表达,诱导CAG大鼠胃粘膜病变的保护性增殖。
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Effect of epidermal growth factor on pathological changes of the gastric mucosa in rats with chronic atrophic gastritis
OBJECTIVE: To study the effect of epidermal growth factor (EGF) on pathological changes of the gastric mucosa in rats with chronic atrophic gastritis (CAG). METHODS: The established CAG rat models were divided into groups A and B. The rats in group A received 10 μg/kg EGF subcutaneously. In group B, rats were subcutaneously injected with the same quantity of normal saline. Twelve weeks later, all rats were killed by cervical dislocation and their gastric mucosa were examined microscopically. RESULTS: The grading of the inflammatory cell infiltration in group A was lower than that in group B (P < 0.01). The thickness of the gastric mucosal gland layer was 215.0 ± 20.7 μm in group A and 139.2 ± 13.8 μm in group B (P < 0.01). The ratio of the thickness of the gastric mucosal glands to that of the muscularis mucosa (L1/L2) was 2.70 ± 0.34 in group A and 1.27 ± 0.27 in group B (P < 0.01). The number of gastric glands in a 1-mm length of mucosal layer was 26.20 ± 1.27 in group A and 19.90 ± 1.78 in group B (P < 0.01). In group A, the gastric glands were rearranged, without signs of malignant proliferation. The width of gastric mucosa expressing proliferating cell nuclear antigen (PCNA) was larger in group A than in group B (77.70 ± 4.16 μm vs 54.40 ± 4.54 μm; P < 0.01). CONCLUSIONS: Epidermal growth factor plays a therapeutic role in reversing gastric mucosal atrophy in rats with CAG. It promotes the expression of PCNA, which induces a protective proliferation in gastric mucosal lesions in rats with CAG.
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