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作 者:王强[1] 吴永贵[1] 吴国仲[1] 齐向明[1] 林辉[1] 钱浩[1] 郝丽[1] 张伯科[1]
机构地区:[1]安徽医科大学第一附属医院肾脏内科,合肥230022
出 处:《安徽医科大学学报》2006年第1期54-57,共4页Acta Universitatis Medicinalis Anhui
基 金:安徽省自然科学基金资助课题(编号:01043703);安徽省教育厅高校中青年学科带头人基金资助课题(编号:522263)
摘 要:目的探讨灯盏花素对糖尿病大鼠肾小管-间质细胞间黏附因子-1(ICAM-1)与单核细胞趋化蛋白-1(MCP-1)表达的影响。方法建立链脲佐菌素(STZ)诱导的大鼠单侧肾切除糖尿病模型,随机分为对照组、模型组、灯盏花素给药组,每组各10只。8周末检测各组尿白蛋白排泄率(AER)与肾组织蛋白激酶C(PKC)活性,应用PAS染色观察肾小管-间质病理形态学,免疫组化方法检测肾小管-间质ED-1、ICAM-1与MCP-1蛋白表达。结果灯盏花素给药组大鼠AER、肾组织PKC活性明显低于模型组(P<0·05),肾小管-间质损伤指数较模型组明显降低(P<0·05)。模型组肾小管-间质ED-1阳性细胞浸润及ICAM-1、MCP-1表达明显高于对照组(P<0·01),灯盏花素可明显缓解这些变化(P<0·05)。结论灯盏花素可明显抑制糖尿病大鼠肾小管-间质巨噬细胞浸润,其机制可能与下调糖尿病肾小管-间质ICAM-1与MCP-1表达有关。Objective To study the effect of breviscapine on intercellular adhesion molecule-1 ( ICAM-1 ) and monoeyte ehemotaetie protein-1 ( MCP-1 ) expression in tubulointerstitium of experimental diabetic rats. Methods Diabetes was induced by injection of streptozotoein after uninephreetomy. Rats were randomly separated into three groups such as control, diabetes, diabetes treated with breviseapine, and each group has 10 rats. 8 weeks after STZ injection, testing 24 hours albumin excretion rate (AER) and the activities of renal tissue protein kinase C (PKC) of each group were observed. The change of tubulointerstitial morphology was observed by PAS pigmentation. ED-1, ICAM-1 and MCP-1 expression in tubulointerstitium were tested by immunohistoehemistry method. Re- sults Increased AER and PKC activities in renal tissue were significantly attenuated by treatment with breviseap- ine. Tubulointerstitial injury index was reduced through breviscapine treatment compared with diabetic group. Increased macrophage recruitment as well as ICAM-1 and MCP-1 protein expression in tubulointerstitium were markedly inhibited by breviscapine in diabetic rats. Conclusion Breviscapine can inhibit increased macrophage recruitment. It may be caused by the suppression of increased expression of ICAM-1 and MCP-1 in tubulointerstitium in diabetic rats.
关 键 词:糖尿病 肾小管-间质 灯盏花素 细胞间黏附因子-1 单核细胞趋化蛋白-1
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