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作 者:林海燕[1] 于佳宁[2] 翟佳丽[1] 赵岩[1] LIN Hai-yan YU Jia-ning ZHAI Jia-li ZHAO Yan(Institute Combining Traditional Chinese and Western Medicine of Binzhou Medical 264003,China Two Gland Surgery of Yantai Affiliated Hospital of Binzhou Medical 264100,China) University, Yantai University, Yantai)
机构地区:[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两腺外科,山东烟台264100
出 处:《中国中西医结合消化杂志》2016年第12期898-901,共4页Chinese Journal of Integrated Traditional and Western Medicine on Digestion
基 金:国家自然科学基金项目(No:81273724);山东省自然科学基金项目(No:ZR2014HL094);山东省2013-2014年度中医药科技发展计划项目(No:2013-249);山东省高等学校优势学科人才团队培育计划
摘 要:[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]Discuss the mechanism of Weiweikang treating chronic atrophic gastritis through detecting the content of IL-6and IL-10 in serum and the expression of NF-Kappa B in gastric mucosal in rats.[Methods]84 SD rats with(180±20)g were randomly divided into normal group and model group.After we verified that the model was successful,the remaining 60 rats in model group were randomly divided into model group,Weiweikang small dose group,medium dose group,large dose group and western medicine group.After treated for 30 days,we measure IL-6and IL-10 levels in rat serum by ELISA method.Takes the stomach organization to embed by paraffin wax.Dye by HE and observes the change of stomach mucous membrane under the light microscope.Measures the expression of NF-Kappa B in gastric mucosal by the Technique of immunity group SP.[Results]Compared with the model group,the content of IL-6in serum and the expression of NF-Kappa B in treatment groups were significantly lower.Weiweikang large dose group was significantly lower compared with small-dose group(P〈0.05).Compared with the model group,the content of IL-10 in serum in treatment groups were significantly higher.Weiweikang large dose group was significantly higher compared with small dose group and medium dose group(P〈0.05).[Conclusion]The possible mechanism of Weiweikang treating chronic atrophic gastritis is inhibiting the signal transduction of NF-Kappa B and stopping the release of IL-6and increasing the release of IL-10 to stop the damage of inflammatory cells on gastric mucosal.At the same time,Weiweikang may achieve the treatment goal through transfering the immunity function of organism to urges the repair of stomach mucous.
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