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作 者:虞文永[1] 丁西平[1] 胡闻[1] 王冬青[1]
机构地区:[1]安徽医科大学附属省立医院消化内科,合肥230001
出 处:《安徽医科大学学报》2014年第12期1751-1754,共4页Acta Universitatis Medicinalis Anhui
基 金:安徽省科技厅年度重点项目(编号:12070403055)
摘 要:目的探讨亮菌口服液对反流液模拟胆汁反流致胃黏膜损伤模型大鼠胃黏膜超氧化物歧化酶(SOD)及白细胞介素-8(IL-8)的影响和超微结构的变化。方法采用反流液灌胃建立胃黏膜损伤大鼠模型,以亮菌口服液干预,观察亮菌口服液对反流液模拟胆汁反流致胃黏膜损伤模型大鼠胃黏膜SOD活性及IL-8含量的影响和超微结构的变化。结果与正常组比较,模型组大鼠胃黏膜SOD活性降低(P<0.05),IL-8含量升高(P<0.05),同时透射电镜观察到模型大鼠胃黏膜细胞间的紧密连接受损,线粒体肿胀,粗面内质网扩张,微绒毛变短或消失。与模型组比较,亮菌口服液组大鼠胃黏膜SOD活性升高,IL-8含量降低。同时亮菌口服液明显改善模型组大鼠胃黏膜的超微结构。结论亮菌口服液具有升高模型大鼠胃黏膜SOD活性,降低IL-8含量的作用,并可修复受损胃黏膜的超微结构,从而保护胃黏膜。Objective To study the influence of SOD & IL-8 and ultrastructural changes on rat bile reflux mucosa model with liangjun oral solution treating.Methods The bile reflux gastritis rats model was established by homemade reflux solution gavage,observing the differences of SOD activity & IL-8 content and ultrastructural changes between liangjun oral solution treating group and the control group.Results Gastric mucosal SOD activity reduced in control group (P < 0.05),IL-8 content increased (P < 0.05).We found the injury of close connection among gastric mucosal cells,mitochondria swelling,rough endoplasmic reticulum expansion,microvilli shorter or lost by transmission electron microscope.Compared with control group,liangjun oral solution could increase experimental bile reflux gastritis rats gastric mucosal SOD activity and reduced the content of IL-8,and significantly repaired the ultrastructure of gastric mucosa in rats.Conclusion Liangjun oral solution could increase the SOD activity,reduce the content of IL-8,repair damaged ultrastructure and prevent gastric mucosa of rat model.
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