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作 者:林辉[1] 吴永贵[1] 齐向明[1] 吴国仲[1] 赵珉[1] 钱浩[1] 周典[1]
机构地区:[1]安徽医科大学第一附属医院肾脏内科,安徽合肥230022
出 处:《中国药理学通报》2005年第6期734-738,共5页Chinese Pharmacological Bulletin
基 金:安徽省自然科学基金资助项目(No01043703);安徽省教育厅高校中青年学科带头人基金资助项目(No522263);安徽省卫生厅第五批科学研究基金资助项目(No2002A004);安徽省教育厅自然基金资助项目(No2005kJ245)
摘 要:目的探讨灯盏花素对糖尿病大鼠肾组织巨噬细胞浸润的影响。方法建立STZ诱导的单侧肾切除糖尿病模型,随机分:对照组、模型组、灯盏花素给药组与MMF给药组。8wk末检测尿白蛋白排泄率(AER)、肾组织蛋白激酶C(PKC)活性,应用免疫组化方法检测肾组织ED1及单核细胞趋化蛋白1(MCP1)与细胞间黏附因子1(ICAM1)表达。结果灯盏花素或MMF给药组大鼠肾重、肾重/体重、AER明显低于模型组(P<0.05)。模型组肾组织细胞浆、细胞膜及细胞总PKC活性明显高于对照组(P<0.01),灯盏花素给药组肾组织PKC活性明显低于模型组(P<0.05),MMF给药组肾组织PKC活性与模型组相比无差异。模型组肾小球ED1阳性细胞数及MCP1、ICAM1表达明显高于对照组(P<0.01),灯盏花素或MMF给药可明显缓解这些变化(P<0.05)。结论灯盏花素对糖尿病大鼠肾脏有明显保护作用,其机制可能部分与抑制肾组织巨噬细胞浸润有关。Aim To study the effect of breviscapine on macrophage recruitment in kidney in diabetic rats. Methods Diabetes was induced by injection of streptozotocin after uninephrectomy. Rats were randomly separated into four groups: control, diabetes, diabetes treated with breviscapine (20 mg·kg -1·d -1 by gavage) and diabetes treated with mycophenolate mofetil( MMF,10 mg -1·kg -1·d -1 by gavage). After 8 weeks, 24 h albumin excretion rate (AER) and PKC activities in renal tissue were detected. Immunohistochemistry for ED-1, monocyte chemotactic protein-1 (MCP-1) and intercellular adhesion molecule-1 (ICAM-1) were determined by streptavidin-biotin comblex technique. Results Increased kidney weight (KW), ratio of kidney weight to body weight (KW/BW) and AER in diabetic rats were significantly attenuated by treatment with breviscapine or MMF (P<0.05). PKC activities in renal tissue were significantly lower in the breviscapine group compared with diabetic group (P<0.05), but treatment with MMF had no effect on PKC activity. Compared with control, glomerular macrophage recruitment as well as MCP-1 and ICAM-1 expression were significantly increased in diabetic rats (P<0.01), and these changes were significantly inhibited by breviscapine or MMF treatment (P<0.05). Conclusion Mechanism of renoprotection of breviscapine may be correlated,at least partly, with suppression on macrophage recruitment in diabetic renal tissue.
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