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[目的]检测中药萎胃康对慢性萎缩性胃炎大鼠血清IL-6,IL-10含量及胃黏膜NF-κB表达的影响,并探讨其作用机制。[方法](180±20)g SD大鼠84只,随机分为正常组14只,造模组70只。确认造模成功后,将造模组剩下的60只大鼠随机分为模型组、萎胃康小、中、大剂量组、西药组。治疗30d后,ELISA法测各组大鼠血清白细胞介素-6(IL-6)、白细胞介素-10(IL-10)含量;取胃组织石蜡包埋,苏木精-伊红染色,光镜下观察胃黏膜变化,免疫组化SP法测胃组织中胃黏膜核转录因子-κB(NF-κB)表达。[结果]各治疗组IL-6和NF-κB的表达较模型组显著降低,其中萎胃康大剂量组较小剂量组显著降低(P<0.05);各治疗组IL-10的表达较模型组显著升高,其中萎胃康大剂量组较中、小剂量组升高明显(P<0.05)。[结论]萎胃康治疗慢性萎缩性胃炎的机制可能是抑制NF-κB介导的信号转导,从而阻止IL-6释放,增加IL-10释放,以阻止炎性细胞对胃黏膜造成的损伤;同时,可调动机体的免疫功能,促使胃黏膜的修复,达到治疗目的。
[Objective] To detect the effect of Weiweikang on serum IL-6, IL-10 and the expression of NF-κB in gastric mucosa in rats with chronic atrophic gastritis and to explore its mechanism. [Method] 84 (180 ± 20) g SD rats were randomly divided into normal group (n = 14) and model group (n = 70). Confirm the success of modeling, the remaining 60 rats in the model group were randomly divided into model group, Weiweikang small, medium and large dose groups, western medicine group. After 30 days of treatment, the contents of IL-6 and IL-10 in serum of rats in each group were measured by ELISA. The gastric tissues were paraffin-embedded, stained with hematoxylin-eosin, The changes of gastric mucosa were observed under light microscope. The expression of NF-κB in gastric mucosa was detected by immunohistochemical SP method. [Results] Compared with the model group, the expression of IL-6 and NF-κB in each treatment group was significantly lower than that in the model group (P <0.05). The expression of IL-10 in each treatment group was significantly lower than that in the model group Group was significantly higher, of which Weiweikang large dose group than the medium and small dose group increased significantly (P <0.05). [Conclusion] The mechanism of Weiweikang in treating chronic atrophic gastritis may be to inhibit the signal transduction mediated by NF-κB, thus preventing the release of IL-6 and increasing the release of IL-10, so as to prevent the damage of inflammatory cells to the gastric mucosa. ; At the same time, the body’s immune function can be mobilized to promote the repair of gastric mucosa, to achieve the purpose of treatment.