Effect of epidermal growth factor on pathological changes of the gastric mucosa in rats with chronic atrophic gastritis
Jiaguo Wu, Jianmin Si, Qian Cao, Wen Lü, Jian Wang, Bingjian Lü, Ning Dai
Abstract
Jiaguo Wu, Jianmin Si, Qian Cao, Wen Lü, Jian Wang, Bingjian Lü, Ning Dai
Abstract
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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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.
Key concepts: Atrophic gastritis, Gastric mucosa, Proliferating cell nuclear antigen, Internal medicine, Epidermal growth factor, Muscularis mucosae, Gastric glands, Pathological