云母对大鼠慢性萎缩性胃炎的预防作用及机制研究

Prevention of isinglass on the chronic atrophic gastritis in rats and its mechanism

目的:研究云母对大鼠慢性萎缩性胃炎的预防作用并探讨其机制。方法:以60%的乙醇、20 mmol/L的去氧胆酸钠和0.1%的氨水在24周建立SD大鼠慢性萎缩性胃炎模型。在造模的同时用云母进行预防实验。实验终期观察鼠胃黏膜大体观及各项病理学指标,并检测血清表皮生长因子和生长激素浓度。结果:云母预防组胃黏膜腺体排列规则,无明显的萎缩现象;胃窦部的胃黏膜炎症级别低于模型组(P<0.01);胃黏膜腺体厚度(L1)和黏膜肌层厚度(L2)之比(L1/L2)高于模型组(P<0.01);单位长度内胃黏膜腺体数目高于模型组(P<0.01)。与正常组无明显差别(P>0.05)。胃窦部黏膜增殖细胞核抗原表达阳性的高度及血清表皮生长因子浓度高于模型组(P<0.01,P<0.05),而生长激素浓度与模型组无明显差别。结论:云母对大鼠慢性萎缩性胃炎的形成有预防作用。减少损伤因子的破坏作用、促进胃黏膜细胞增殖及内源性的表皮生长因子分泌,可能是其重要作用机制。

AIM： To evaluate the effect of isinglass on chronic atrophic gastritis （CAG） in rats and its mechanism. METHODS： An animal model of CAG in accordance with the previous experience of combined administration of 60% ethanol, 20 mmol/L sodium deoxycholate and 0. 1% ammonia water was established in SD rats. Isinglass was used as preventive therapy while we were establishing CAG rat model. Finally all the rats were executed and pathologic changes of the gastric mucosa were studied by gross appearance and microscopy and serum epidermal growth factor （EFG） and growth hormone（GH） contents were tested. RESULTS： In each isinglass prevention group, inflammation grade of gastric antrum was less than that in model group （P 〈 0.01 ） while the mean ratio of the thickness of gastric mucosal gland and muscularis mucosa （L1/L2）, the number of gastric glands in 1 mm lengths of mucosal layer in longitudinal sections were much better than those in model group （P 〈0.01 ）. They were very close to normal control group （P 〉0. 05）. The expression of proliferating cell nuclear antigen （PCNA） in gastric mucosa and serum EFG level were higher than those in model group （P 〈 0. 01, P 〈0. 05）, but serum GH content showed no different between isinglass prevention group and model group. CONCLUSION： Isinglass preventes the gastric mucosal atrophy in the CAG model. Its mechanism may be related to the effects of decreasing the gastric mucosal damage, promoting the cell proliferation and increasing of internal EFG secretion.