逆萎康对慢性萎缩性胃炎大鼠胃黏膜组织P16和TGF-β1表达影响  

EFFECT OF NIWEIKANG ON EXPRESSIONS OF P16 AND TGF-β1 IN GASTRIC MUCOSA OF RATS WITH CHRONIC ATROPHIC GASTRITIS

作　　者：梁坤[1] 张红珠[1] 周广玺[1] 孙向红[2] 王辉明[2] 张翠萍[1] 

机构地区：[1]青岛大学医学院附属医院消化内科,山东青岛266003 [2]青岛大学医学院附属医院药剂科,山东青岛266003

出　　处：《青岛大学医学院学报》2014年第1期37-39,42,共4页Acta Academiae Medicinae Qingdao Universitatis

摘　　要：目的研究逆萎康干预治疗对慢性萎缩性胃炎(CAG)大鼠胃黏膜中P16蛋白和TGF-β1表达的影响。方法健康雄性Wistar大鼠70只,随机分为正常对照组、CAG模型组和逆萎康干预组,采用幽门螺杆菌、乙醇-水杨酸综合造模法制作CAG大鼠模型,逆萎康干预组在造模过程中给予逆萎康干预治疗25周。观察各组大鼠胃黏膜形态和镜下改变,并应用免疫组织化学方法检测各组大鼠胃黏膜中P16和TGF-β1蛋白的表达。结果逆萎康干预组大鼠胃黏膜腺体排列规整,黏膜层较CAG模型组厚。正常对照组和逆萎康干预组P16蛋白阳性表达率明显高于CAG模型组(χ2=17.733、9.823,P<0.05);TGF-β1蛋白阳性表达率明显低于CAG模型组(χ2=21.390、16.546,P<0.05)。正常对照组和逆萎康干预组间P16和TGF-β1蛋白阳性表达率比较差异无显著性(P>0.05)。结论逆萎康能有效保护胃黏膜,防止CAG的发生和发展,其作用机制可能与上调P16蛋白和下调TGF-β1蛋白的表达有关。Objective To investigate the effect of Niweikang intervention treatment on expressions of P16 protein and TGF-β1 in gastric mucosa of rats with chronic atrophic gastritis （CAG）. Methods Seventy healthy male Wistar rats were ran- domly divided into normal control group, CAG model group and Niweikang-treatment group. A CAG model in rat was created by using a synthetic method with H. pylori and ethanol salicylate. The rats in Niweikang-treatment group reeeived Niweikang inter- vention for 25 weeks during the creation of the model. The general morphology and microscopic changes of gastrie mucosa were ob- served, the expressions of P16 protein and TGF-β1 in the mucosa were detected by immunohistochemistry. Results The gland arrangement of gastric mucosa in the Niweikang-treatment group was neat, and its mucous layer was thicker than that in CAG model group. The positive expression rate of P16 protein in normal control group and Niweikang-treatment group was higher than that in CAG model group （X2 = 17.733,9.823;P〈0.05）, and that of TGF-β1 was lower （X2= 21.390,16.546;P〈0.05）. The difference of expression of P16 protein and TGF-β1 between normal control group and Niweikang-treatment group was not significant （P〉0.05）. Conclusion Niweikang can effectively protect gastric mucosa, prevent the occurrence and development of CAG. The mechanism might be related to up regulation of P16 protein and down-regulation of TGF-β1.

关 键 词：胃炎 萎缩性 基因 p16 转化生长因子B 逆萎康 

分 类 号：R573.3[医药卫生—消化系统]