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作 者:刘芳[1] 史迎莉[2] 张晓芹[1] 许小凡[2] 陈瑜[1] 张红[2]
机构地区:[1]陕西中医药大学基础医学院,西安712046 [2]陕西中医药大学医学科研实验中心,西安712046
出 处:《中国应用生理学杂志》2015年第5期477-480,共4页Chinese Journal of Applied Physiology
基 金:国家自然科学基金(81102725);陕西省中医药管理局项目(jc10);陕西省教育厅自然科学基金资助项目(11JK0717;14JK1189)
摘 要:目的:探讨胰腺氧化炎症级联反应在二氯二丁基酯(DBTC)联合乙醇诱发小鼠慢性胰腺炎胰腺纤维化进展中的作用及机制。方法:健康昆明小鼠36只,随机分为两组(n=18):对照组和模型组,模型组经尾静脉一次性注射DBTC(8 mg/kg)后加饮10%乙醇饲喂诱发慢性胰腺炎。造模后2、4、8周处死动物,HE及Masson胶原纤维染色观察胰腺组织的病理学改变及纤维化程度,免疫组织化学法检测F4/80的表达;制备胰腺组织匀浆检测超氧化物歧化酶(SOD)、丙二醛(MDA)、髓过氧化物酶(MPO)的变化。结果:模型组小鼠HE染色和Masson染色显示造模2周后可见成纤维细胞出现、巨噬细胞(F4/80阳染)浸润,4周及8周巨噬细胞浸润增加、伴随胰腺实质明显减少并被大量纤维组织取代。胰腺组织匀浆SOD活性逐渐降低,MDA和MPO逐渐升高,与对照组同时间点相比,有显著性差异(P<0.05)。结论:DBTC尾静脉注射联合饮用乙醇可以成功建立小鼠慢性胰腺炎胰腺纤维化模型,氧化炎症级联反应在胰腺纤维化进展中发挥重要的作用。Objective: To explore the role and mechanism of oxidative inflammatory cascade in pancreatic fibrosis progression of chronic pancreatitis(CP) in mice induced by dibutyhin dichloride (DBTC) plus ethanol. Methods: Thirty-six KM mice were randomly divided into 2 groups( n = 18) :control group and model group(DBTC combined with ethanol). The mice in model group were intravenously injected with DBTC (8 mg/kg) in tail vein and drink 10% ethanol. After modeling 2 weeks, 4 weeks and 8 weeks, the mice were anesthetized and sacri- ficed, the pathological changes and the degree of fibrosis in the pancreas were observed by HE and Masson staining, the F4/80 expression level were detected by immunohistochemistry, the content of superoxide dismutase( SOD ), malondialdehyde(MDA) and myeloperoxidase( MPO )were measured in the pancreatic homogenates. Results: The fibroblasts and macrophages (f4/80 positive staining) could be seen obviously in pan- creas of model group at 2 weeks. At 4 weeks and 8 weeks, macrephages infiltration increased and pancreatic tissue was substituted by the pro- liferation of fibrosis significantly. At every time-point, in pancreatic homogenates SOD was decreased, MDA and MPO markedly increased. There was significant differences between two groups( P 〈 0.05). Conclusion: DBTC injection joint ethanol drinking can successfully establish the model of chronic pancreatitis and pancreatic fibrosis in mice. Oxidative inflammatory cascade plays an important role in the progression of pancreatic fibrosis.
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