鼠慢性萎缩性胃炎胃黏膜形态特征和细胞增殖调控因子变化研究  

Studies of the pathologic change of gastric mucosa and regulating factors of cell proliferation in rats with experimental chronic atrophic gastritis

作　　者：姒健敏[1] 王良静[1] 陈淑洁[1] 朱方石 钱云[1] 徐妙[1] 

机构地区：[1]浙江大学邵逸夫临床医学研究所胃肠病研究室,杭州310016

出　　处：《中华消化杂志》2004年第8期476-479,共4页Chinese Journal of Digestion

基　　金：浙江省科技厅资助项目 ( 2 0 0 1A2 10 )

摘　　要：目的　研究鼠慢性萎缩性胃炎 (CAG)的病理变化和细胞增殖分子调控变化 ,探讨CAG发生的可能机制。方法　综合采用 6 0 %乙醇或 2 %水杨酸钠、2 0mmol/L去氧胆酸钠和 0 .1%氨水建立大鼠CAG模型。观察大鼠胃黏膜病理组织变化和黏液分泌功能。测定大鼠血清表皮生长因子 (EGF)和前列腺素E2 (PGE2 )水平 ,免疫组化分析EGF受体 (EGFR)、C erbB2、P5 3、P16和Bcl 2蛋白的表达。结果　鼠CAG胃窦黏膜的炎症改变明显 ,腺体数目和厚度显著降低 ,部分大鼠出现肠上皮化生。扫描电镜可见胃黏膜破溃、细胞脱落。鼠CAG胃黏膜氨基己糖和血清PGE2较正常组显著下降 (P <0 .0 5 )。CAG大鼠血清EGF水平为 (2 .2 4± 0 .83) μg/L ,较正常大鼠的 (0 .6 1± 0 .2 8) μg/L显著升高 (P <0 .0 5 )。鼠CAG胃组织EGFR和C erbB2阳性表达率分别为 4 5 %和 70 % ,正常大鼠均无表达 (P <0 .0 5 )。正常大鼠P16蛋白表达率为 75 % ,显著高于模型大鼠的 10 % (P <0 .0 5 ) ,模型大鼠Bcl 2蛋白表达率为5 0 % ,高于正常大鼠的 10 % (P <0 .0 5 )。CAG和正常大鼠的P5 3蛋白表达率分别为 30 %和 10 % ,差异无显著性 (P >0 .0 5 )。结论　鼠CAG的发生与多种致病因素破坏胃黏膜屏障 ,胃黏膜细胞增殖和凋亡失衡有关。Objective To assess pathologic and molecular regulating changes of cell proliferation of gastric mucosa in rats with chronic atrophic gastritis (CAG) and approach the possible mechanisms of the disease. Methods Rats were administered with 60% alcohol (2% Salicylate Sodium), 20 mmol/L sodium deoxycholate and 0.1% ammonia water to establish CAG model. The pathological change and mucin secretion were evaluated. The level of the serum prostaglandin E (PGE)2 and endothelial growth factor (EGF) were measured with radioimmunoassay. The immunohistochemistry was used to detect the expression of EGF receptor (EGFR), C-erbB2, P53, P16 and Bcl-2. Results Compared with normal rats, the grade of inflammatory cell infiltration in gastric mucosa in CAG rats was elevated, whereas the thickness and number of gastric gland were significant lower. Scanning electromicroscopy showed the cells rupture and injury of barrier of gastric mucosa. The levels of haxosamine in gastric mucosa and PGE2 in serum were lower in CAG rats than in normal rats (P<0.05). Compared with normal level of (0.61±0.28) μg/L, EGF in CAG in serum (2.24± 0.83) μg/L was significant higher (P<0.05). The immunohistochemistry studies showed that the expression of EGFR and C-erbB2 were 45% and 70% respectively in CAG rats, while no expression in normal rats (P< 0.05). The expression rate of P16 was 75% in normal rats,which was 10% higher than that in CAG rats (P<0.05). Compared with the rats in normal group, Bcl-2 expression was higher in CAG (10% vs. 50% P<0.05). There was no significant difference in expression of P53 between CAG and normal group (30% vs. 10%, P>0.05).Conclusion The pathogenesis of CAG in rats was related with the damage of barrier in gastric mucosa and the imbalance of cell proliferation and apoptosis.

关 键 词：鼠 慢性萎缩性胃炎 胃黏膜 形态特征 细胞增殖 调控因子 CAG 病理变化 

分 类 号：R573.3[医药卫生—消化系统]