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作 者:顾海峪[1] 卢建华[1] 傅君舟[1] 梁鸣[1] 阳晓[2]
机构地区:[1]广州市第一人民医院急诊科,510180 [2]中山大学附属第一医院,广州市510080
出 处:《实用医学杂志》2005年第17期1866-1868,共3页The Journal of Practical Medicine
基 金:国家自然科学基金资助项目(编号:30271668);广东省医学科研基金资助项目(B2003122);广东省中医药局立项科研基金资助项目(编号:403029)
摘 要:目的:观察慢性移植物抗宿主病(cGVHD)狼疮样肾炎小鼠模型肾组织中钙调神经磷酸酶(CaN)活性,及FK506的调控作用。方法:cGVHD狼疮样小鼠模型随机分两组:模型组和FK506治疗组,每组10只。采用发色底物法检测CaN活性。结果:(1)模型组肾小球硬化指数及小管间质损伤总积分显著高于正常组(P<0.001);FK506治疗后肾脏病变明显减轻;(2)模型组肾组织中CaN活性显著增强,与正常对照组肾组织CaN活性相比差异有显著性(P<0.001);FK506组肾组织中CaN活性显著回降(P<0.05);(3)狼疮样肾炎小鼠肾组织中CaN活性与肾小球硬化指数及小管间质损伤总积分呈正相关关系(r1=0.626,P<0.01;r2=0.772,P<0.05)。结论:cGVHD狼疮样小鼠肾组织CaN异常活化,FK506在改善肾组织病理改变的同时,对CaN活性亦起抑制作用。Objective To investigate the effect of FK506 on the Calcineurin (CAN) activation in kidney of lupeid model mice. Methods Chronic graft-versus-host disease(cGVHD) murine lupus nephritis models were used and divided into two groups, the model group was un-treated and the other group treated with FK506. The assay conditions for CaN in extracts from mouse renal tissue were extensively investigated. Results (1) The glomerular sclerosis index (GSI) and tubulointerstitial injury score were significantly increased in lupoid mice (P 〈 0.001), but that in the FK506 group was different from the model mice significantly( P 〈0. 001). (2) We observed specific increase in CaN activity was distinctly higher in kidney as compared with in those from control mice (P 〈 0. 001). CaN activity was decreased in kidney of FK506 group than model mice (P 〈 0.05). (3) The activation of CaN in model kidney was significantly associated with GSI and tubulointerstitial injury score, respectively( r=0. 626, P 〈 0. 01;r2 = 0. 772, P 〈 0.05). Conclusion FK506 inhibit the activation of CaN in kidney of lupoid mice and alleviate the renal pathologic changes.
关 键 词:狼疮肾炎 FK506 钙调神经磷酸酶 钙调神经磷酸酶活性 狼疮样肾炎 鼠肾组织 慢性移植物抗宿主病 小鼠模型 CGVHD 肾小球硬化
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