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萎胃康颗粒对慢性萎缩性胃炎大鼠胃黏膜上皮细胞PCNA和EGFR蛋白表达的影响
引用本文:林海燕,赵岩,于佳宁.萎胃康颗粒对慢性萎缩性胃炎大鼠胃黏膜上皮细胞PCNA和EGFR蛋白表达的影响[J].中国实验方剂学杂志,2012,18(17):179-182.
作者姓名:林海燕  赵岩  于佳宁
作者单位:1. 滨州医学院中西医结合学院,山东烟台,264003
2. 滨州医学院烟台附属医院,山东烟台,264100
基金项目:国家自然科学基金项目(81072782);山东省科技发展计划项目(2011YD19012)
摘    要:目的:探讨萎胃康颗粒对大鼠慢性萎缩性胃炎(CAG)的治疗作用及其机制.方法:90只SD大鼠随机取出18只为正常对照组,其余鼠造模后随机分为4组,模型组、萎胃康高、低剂量组、三九胃泰组均采用多重刺激复制大鼠CAG模型.在造模成功后分别ig萎胃康6,3 g·kg-1,三九胃泰1.6g·kg-1,0.9%的生理盐水20 mL·kg-1.用药30 d后HE染色、透射电镜观察大鼠胃黏膜萎缩情况,免疫组化法观察胃黏膜上皮细胞中增殖细胞核抗原(PCNA)和表皮生长因子受体(EGFR)的表达.结果:光镜和电镜下均显示,萎胃康高、低剂量组胃黏膜病理变化比模型组明显减轻.模型组PCNA标记指数44.96%和EGFR的平均吸光度(A)0.183 ±0.030,明显高于正常组PCNA标记指数29.30%和EGFR的4 0.125±0.039.萎胃康高、低剂量组PCNA标记指数分别为29.58%,29.97%,EGFR的A分别为0.100±0.023,0.104±0.027,与模型组比较,表达降低(P <0.05或P<0.01).结论:中药萎胃康颗粒对慢性萎缩性胃炎大鼠胃黏膜有明显修复作用,其作用机制可能是通过抑制胃黏膜PCNA和EGFR的过度表达而抑制细胞增殖和恶性转化实现的.

关 键 词:慢性萎缩性胃炎  萎胃康  上皮细胞中增殖细胞核抗原  表皮生长因子受体
收稿时间:2011/6/28 0:00:00

Influences of Weiweikang Granule on PCNA, EGFR of Gastric in Rats with Chronic Atrophic Gastritis
LIN Hai-yan,ZHAO Yan and YU Jia-ning.Influences of Weiweikang Granule on PCNA, EGFR of Gastric in Rats with Chronic Atrophic Gastritis[J].China Journal of Experimental Traditional Medical Formulae,2012,18(17):179-182.
Authors:LIN Hai-yan  ZHAO Yan and YU Jia-ning
Institution:Binzhou Medical University,Yantai 264003,China;Binzhou Medical University,Yantai 264003,China;Yantai Hospital Affiliated to Binzhou Medical University, Yantai 264100,China
Abstract:Objective: To study the influences of Weiweikang granule(WWKG) on the expression of proliferating cell nuclear antigen (PCNA), epidermal growth factor receptor (EGFR) of gastric mucosa with chronic atrophic gastritis(CAG), and evaluate the possible mechanisms. Method: Ninety SD rats were randomly divided into five groups. The high dose WWKG group, low dose WWKG group, Sanjiu Weitai granule(SJWTG) group and model group.The multiple stimulations were used to duplicate the CAG model. After modeled successfully, the high dose WWKG group, low dose WWKG group, SJWTG group and model group were intragastrically injected(ig) with WWKG at dose of 6, 3 g·kg-1, and SJWTG at dose of 1.6 g·kg-1, respectively and normal saline(0.9%)at dose of 20 mL·kg-1. After 30 days, the rats'stomach mucous membrane atrophy situation was observed with the help of light microscopy and transmission electron microscopy and the expression of PCNA and EGFR were observed with immunohistochemical method. Result: The light microscopy and electron microscopy examination showed that the pathological changes of gastric mucosa in large dose WWKG group and small dose WWKG group were significantly milder than those in the model group. Compared with the control group, the expression of PCNA labeling index(LI 44.96%)and EGFR(average obsorbance,A0.183 ±0.030) in the model group was higher than the normal group (LI 29.30%, A 0.125±0.039)obviously(P<0.01).Compared with the model group, the expression of PCNA and EGFR in large dose WWKG group(LI 29.58%,A 0.100±0.023)and small dose WWKG group (LI 29.97%, A 0.104±0.027)was significantly lower(P<0.05 or P<0.01). Conclusion: WWKG can significantly repair gastric mucosa of rats with CAG and its mechanism may be actualized by decreasing the expression of PCNA and EGFR and restraining cell proliferation and malignant transformation.
Keywords:chronic atrophic gastritis  Weiweikang granul  PCNA  EGFR
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