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作 者:杜燕[1] 易受乡[1] 林亚平[1] 洪金标[1] 彭宏[1] 黄芸[1] 常小荣[1] 吴焕淦[2]
机构地区:[1]湖南中医药大学针灸推拿学院,长沙410007 [2]上海市针灸经络研究所,上海200030
出 处:《上海针灸杂志》2010年第5期269-272,共4页Shanghai Journal of Acupuncture and Moxibustion
基 金:国家自然科学基金(NO.30772707);国家重点基础研究发展计划(2009CB522904);教育部博士点科基金资助项(20070541003)
摘 要:目的探讨艾灸对急性胃黏膜损伤的保护作用及其炎症反应的抑制机制。方法健康SPF级SD大鼠,随机分对照组、模型组、艾灸组和艾灸非穴位组。采用无水乙醇灌胃制备急性胃黏膜损伤模型。艾灸足三里、中脘穴,按GUTH法计算胃黏膜损伤指数(UI),HE染色观察胃黏膜组织形态学变化,免疫组织化学法检测胃黏膜细胞中HSP70的表达,放免法测定血清中炎性细胞因子的含量。结果与对照组比较模型组胃黏膜损伤指数、血清中炎性细胞因子含量明显升高(P<0.01),胃黏膜组织炎性浸润明显。与模型组相比,艾灸组胃黏膜损伤指数、血清中炎性细胞因子含量明显降低(P<0.01或P<0.05),胃黏膜组织形态较为完好,HSP70大量表达(P<0.01)。结论艾灸足三里、中脘穴对大鼠急性胃黏膜损伤具有一定的保护作用,其机制可能与诱导机体产生大量HSP70抑制炎性细胞因子的释放有关。Objective To explore the protective effect of moxibustion against acute gastric mucosal injury and the mechanism of its inhibition of inflammatory reaction. Methods Healthy SPP class SD rats were randomly allocated to control, model, moxibustion and non-acupoint moxibustion groups. A model of gastric mucosal injury was made by gavage of absolute alcohol. Moxibustion was performed on points Zusanli and Zhonhwan. Gastric mucosal injury index was calculated by the GUTH method. Histomorphologic changes in gastric mucosa were observed by HE staining. The expression of HSP70 in gastric mucosal cells was examined by an immunohistochemical method. Serum inflammatory cytokine content was measured by radioimmunoassay. Results Gastric mucosal injury index and serum inflammatory cytokine content increased markedly (P 0.01) and inflammatory infiltration was obvious in the model group compared with the control group. Gastric mucosal injury index and serum inflammatory cytokine content decreased markedly (P〈0.01 or P〈0.05), the form of gastric mucosa was less damaged and HSP70 was expressed in large amounts (P〈0.01) in the moxibustion group compared with the model group. Conclusion Moxibustion on points Zusanli and Zhongwan has a certain protective effect against acute gastric mucosal injury. Its mechanism may be related to its inducing the production of large amounts of HSP70 in the body to inhibit the release of inflammatory cytokines.
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