中文摘要：

目的：探讨穴位埋线对慢性萎缩性胃炎（CAG）模型大鼠胃黏膜组织IKKβ、IκB、NF-κB表达的影响。方法：将50只SD大鼠随机分为空白组10只和造模组40只,造模组采用自由饮用浓度为100μg/L的MNNG溶液,同时配合饥饱失常法进行造模,造模成功后随机分为模型组10只,埋线组10只,假埋线组10只。所有大鼠正常条件下喂养,埋线组选取大鼠＂足三里＂、＂中脘＂、＂脾俞＂穴行埋线疗法治疗,假埋线组仅用埋线针针刺上述穴位治疗,每10d治疗1次,共治疗6次。采用免疫组化检测各组大鼠胃黏膜组织IKKβ、IκB、NF-κB表达情况,并采用图像分析系统行半定量分析。结果：与空白组比较,模型组和假埋线组大鼠胃黏膜组织IKKβ、IκB、NF-κB表达显著升高（P〈0.01）,埋线组表达升高（P〈0.05）;与模型组比较,埋线组表达显著降低（P〈0.01）,假埋线组则差异无统计学意义。结论：穴位埋线疗法可以抑制IKKβ活化,进而抑制IκB降解,从而降低NF-κB活化水平,对慢性萎缩性胃炎具有较好的治疗作用。

英文摘要：

Objective： To explore the impact Of catgut embedding in points therapy on expression of IKK[], IrB, NF- ~~B in gastric mucosa of chronic atrophic gastritis （CAG） model rats. Methods： 50 SD rats were randomly divided into the normal control group with 10 rats and the model group with 40 rats. With irregular diet method, the model group was modeled by drinking MNNG solution freely with concentration of 100μg/L. After the CAG was detected by immunohistochemeical detection and analyzed half-quantitatively model was confirmed succeeded, they were randomly divided into the model group, catgut embedding group and fake catgut embedding group, 10 rats with each group. All rats were fed under normal conditions. The embedding group was treated by embedding catgut in the points of Zusanli （ST36）, Zhongwan （RNI2） and Pishu （DL20） every 10 days, 6 times in total, while those in fake catgut embedding group were treated by needling with catgut embedding needle. The IKKβ, IκB and NF- κB expression in gastric mucosa were analyzed by image analysis system. Results： Compared with the normal group, the IKKβ, IκB and NF-κB expression in the model group and the fake catgut embedding group were significantly increased （P〈0.01）, and increased in the catgut embedding group （P〈0.05）. Compared with the model group, the expression in catgut embedding group was significantly lower （P〈0.01）, while the fake catgut embedding group showed no statistical difference. Conclusion： Catgut embedding in points therapy can inhibit the activation of IKKβ which inhibiting the degradation of lκB and results in reducing the level of NF-κB activation. Therefore, this therapy has a better therapeutic effect on chronic atrophic gastritis.