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[The effect of epidermal growth factor on the pathologic changes of gastric mucosa in SD rats with chronic atrophic gastritis].

Sherry Jingjing Wu, Jianmin Si, Qin Cao, Lu Wang, Jian-Yu Weng, Bingjie Lu, Ning Dai

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Abstract

OBJECTIVE: To study the effect of epidermal growth factor (EGF) on the pathologic changes of gastric mucosa in rats with chronic atrophic gastritis(CAG). METHODS: The established rat models of CAG were divided into therapy group and control group. The rats in the therapy group received EGF 10 microg/kg subcutaneously (SC), whereas these in the control group the same volume of normal saline SC. 12 weeks later, all rats were killed by cervical dislocation and their gastric mucosa were examined with microscope. RESULTS: The grade of inflammatory cell infiltration in the therapy group was lower than that in the control group (P < 0.01). The thickness of gastric mucosal gland layer was (215.0 +/- 20.7) microm in the therapy group and (139.2 +/- 13.8) microm in the control group (P < 0.01). The ratio of the thickness of gastric mucosal glands and muscularis mucosa(L(1)/L(2)) was 2.70 +/- 0.34 in the therapy group and 1.27 +/- 0.27 in the control group (P < 0.01). The number of gastric glands in 1 mm length of mucosal layer was 26.20 +/- 1.27 in the therapy group and 19.90 +/- 1.78 in the control group (P < 0.01). In the therapy group, the gastric glands were rearranged in order, without signs of malignant proliferation. The width of the expression of proliferating cell nuclear antigen (PCNA ) of gastric mucosa was higher in the therapy group than in the control group [(77.70 +/- 4.16) microm vs (54.40 +/- 4.54) microm, P < 0.01]. CONCLUSIONS: EGF played a therapeutic role in reversing the gastric mucosal atrophy of the rats with CAG. It promoted the expression of PCNA, which induced a protective proliferation of the gastric mucosal lesions in the rats with CAG.

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OBJECTIVE: To study the effect of epidermal growth factor (EGF) on the pathologic changes of gastric mucosa in rats with chronic atrophic gastritis(CAG). METHODS: The established rat models of CAG were divided into therapy group and control group. The rats in the therapy group received EGF 10 microg/kg subcutaneously (SC), whereas these in the control group the same volume of normal saline SC. 12 weeks later, all rats were killed by cervical dislocation and their gastric mucosa were examined with microscope. RESULTS: The grade of inflammatory cell infiltration in the therapy group was lower than that in the control group (P < 0.01). The thickness of gastric mucosal gland layer was (215.0 +/- 20.7) microm in the therapy group and (139.2 +/- 13.8) microm in the control group (P < 0.01). The ratio of the thickness of gastric mucosal glands and muscularis mucosa(L(1)/L(2)) was 2.70 +/- 0.34 in the therapy group and 1.27 +/- 0.27 in the control group (P < 0.01). The number of gastric glands in 1 mm length of mucosal layer was 26.20 +/- 1.27 in the therapy group and 19.90 +/- 1.78 in the control group (P < 0.01). In the therapy group, the gastric glands were rearranged in order, without signs of malignant proliferation. The width of the expression of proliferating cell nuclear antigen (PCNA ) of gastric mucosa was higher in the therapy group than in the control group [(77.70 +/- 4.16) microm vs (54.40 +/- 4.54) microm, P < 0.01]. CONCLUSIONS: EGF played a therapeutic role in reversing the gastric mucosal atrophy of the rats with CAG. It promoted the expression of PCNA, which induced a protective proliferation of the gastric mucosal lesions in the rats with CAG.

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Available abstract

OBJECTIVE: To study the effect of epidermal growth factor (EGF) on the pathologic changes of gastric mucosa in rats with chronic atrophic gastritis(CAG). METHODS: The established rat models of CAG were divided into therapy group and control group. The rats in the therapy group received EGF 10 microg/kg subcutaneously (SC), whereas these in the control group the same volume of normal saline SC. 12 weeks later, all rats were killed by cervical dislocation and their gastric mucosa were examined with microscope. RESULTS: The grade of inflammatory cell infiltration in the therapy group was lower than that in the control group (P < 0.01). The thickness of gastric mucosal gland layer was (215.0 +/- 20.7) microm in the therapy group and (139.2 +/- 13.8) microm in the control group (P < 0.01). The ratio of the thickness of gastric mucosal glands and muscularis mucosa(L(1)/L(2)) was 2.70 +/- 0.34 in the therapy group and 1.27 +/- 0.27 in the control group (P < 0.01). The number of gastric glands in 1 mm length of mucosal layer was 26.20 +/- 1.27 in the therapy group and 19.90 +/- 1.78 in the control group (P < 0.01). In the therapy group, the gastric glands were rearranged in order, without signs of malignant proliferation. The width of the expression of proliferating cell nuclear antigen (PCNA ) of gastric mucosa was higher in the therapy group than in the control group [(77.70 +/- 4.16) microm vs (54.40 +/- 4.54) microm, P < 0.01]. CONCLUSIONS: EGF played a therapeutic role in reversing the gastric mucosal atrophy of the rats with CAG. It promoted the expression of PCNA, which induced a protective proliferation of the gastric mucosal lesions in the rats with CAG.

Key concepts: Medicine, Gastric mucosa, Atrophic gastritis, Internal medicine, Epidermal growth factor, Gastroenterology, Proliferating cell nuclear antigen, Saline

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[The effect of epidermal growth factor on the pathologic changes of gastric mucosa in SD rats with chronic atrophic gastritis]. — Research Paper | ScholarLens