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作 者:马建丽[1] 黎春彤[1] 李翔[1] 刘茜[1] 梁璐 朴晋华
机构地区:[1]解放军总医院第一附属医院,北京100048 [2]山西省心血管病医院,山西太原030024 [3]山西省食品药品检验所,山西太原030001
出 处:《解放军药学学报》2017年第2期138-141,共4页Pharmaceutical Journal of Chinese People's Liberation Army
摘 要:目的观察扁咽口服液对急性咽炎大鼠的疗效及其抑制炎症因子过表达的作用。方法选取SD大鼠56只,随机分成7组:空白对照组、模型组、自然恢复组、阳性对照组、扁咽口服液低、中、高剂量组。除空白对照组外,其余6组咽部黏膜注射乙型溶血性链球菌建立急性咽炎动物模型,造模成功后处死模型组;给药组分别给予扁咽口服液1.87、3.73、7.46g·kg^(-1)和注射用氨苄西林钠0.6g·kg^(-1),空白对照组和自然恢复组均给予等容量的灭菌水,连续给药5d。末次给药后取大鼠咽部组织及股动脉血,观察各组咽部组织的病理形态学变化,免疫组化方法观察咽喉组织基质金属蛋白-9表达水平,用ElASA方法测定血清IL-1β、TNF-α表达。结果与自然恢复组相比,扁咽口服液高剂量能不同程度改善模型大鼠咽部组织形态,血清中IL-1β、TNF-α表达均显著降低(P<0.05),咽喉组织中基质金属蛋白-9表达亦明显减少。结论扁咽口服液对急性咽炎大鼠有较好的治疗作用,其机制可能是通过调节炎症因子的过度表达和抑制咽部组织基质金属蛋白-9表达,进而控制咽部病理改变而实现的。Objective To observe the effect of Bianyanoral solution on rat models of acute pharyngitis and its regulation of inflammatory factors.Methods Fifty-six SD rats were randomly divided into seven groups:blank control group,model group,natural recovery group,low,medium and high dosage Bianyan oral solution groups and positive control group.The rat model of acute pharyngitis was established by directly applying beta hemolytic streptococcus into the pharyngeal mucos in each group except the blank control group.Rats in the model group were sacrificed while the other six groups were given ig Bianyan oral solution(1.87,3.73,7.46g·kg^-1),ampicillin sodium solution(0.6g·kg^-1)or water for 5days respectively.Pharyngeal tissues and femoral arterial blood were taken after the last dose.Changes in pharyngeal pathological morphology of pharyngeal tissues,matrix metallo proteinases-9expression and serum IL-1β,TNF-αexpression were observed.Results Compared to the natural recovery group,the pathological changes of model group with acute pharyngitis improved to different degrees and the expressions of IL-1β,TNF-αin serum and matrix metallo proteinases-9 in the pharyngeal mucos were obviously reduced by Bianyanoral solution at high-and mid-doses.Conclusion Bianyan oral solution has a good curative effect on acute pharyngitis,and the mechanism may be related to the regulation of the expressions of matrix metallo proteinases-9,IL-1β and TNF-α.
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