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雷公藤多苷对阿霉素肾病大鼠足细胞病变的影响
引用本文:王军建,胡锐,毛云英,周南.雷公藤多苷对阿霉素肾病大鼠足细胞病变的影响[J].陕西医学杂志,2011,40(9):1119-1122,F0003.
作者姓名:王军建  胡锐  毛云英  周南
作者单位:1. 西安市儿童医院急诊科,西安,710002
2. 陕西省交通医院儿科
摘    要:目的:探讨雷公藤多苷(TG)对微小病变型肾病的疗效及其对足细胞病变的影响。方法:将27只SD大鼠随机分为3组,模型组通过对大鼠尾静脉一次性注射,建立阿霉素肾病(AIN)模型;雷公藤多苷治疗组每天给予雷公藤多苷50mg/kg灌胃治疗;对照组给予等量生理盐水注射。分别在第2、5、8周末收集大鼠尿标本,检测24h尿蛋白排泄量。8周末处死大鼠,留取血、肾脏标本,检测血生化指标;并行肾组织光镜和电镜观察肾小球病变和足突超微结构。免疫组化染色观察足细胞裂孔膜分子Nephrin和CD2AP表达和分布变化。结果:1尿蛋白:用雷公藤多苷治疗3周后,模型组大鼠尿蛋白即可显著降低,至6周后,雷公藤多苷治疗组大鼠尿蛋白进一步降低,与模型组大鼠相比有极显著性差异(P<0.01)。2足细胞病变:经雷公藤多苷治疗6周后,可见足细胞的足突损伤比对照组明显减轻,足突融合显著改善,大部分足细胞的足突形态基本恢复正常。3足细胞裂孔膜蛋白的变化:经雷公藤多苷治疗6周后,足细胞Nephrin和CD2AP的表达比AIN大鼠有明显增加(P<0.01),分布上的异常得到纠正,基本恢复成连续的线样分布。结论:雷公藤多苷可以保护和修复AIN大鼠肾小球足细胞损伤,减少足突的融合,增加肾小球足细胞Nephrin和CD2AP的表达,减少尿蛋白,从而缓解肾组织慢性炎症变化。

关 键 词:肾病综合征/化学诱导  肾病综合征/药物作用  肾病综合征/病理学

Effect of triptergium glycosides on podocyte injury in rats with Adriamycin- induced nephropathy
Wang Junjian Hu Rui Mao Yunying et al.Effect of triptergium glycosides on podocyte injury in rats with Adriamycin- induced nephropathy[J].Shaanxi Medical Journal,2011,40(9):1119-1122,F0003.
Authors:Wang Junjian Hu Rui Mao Yunying
Institution:Wang Junjian Hu Rui Mao Yunying et al Department of Emergency,Xi'an Children's Hospital(Xi'an 710002)
Abstract:Objectives:To explore the therapeutic effect and mechanism of triptergium glycosides(TG) on minimal change nephrotic syndrome using Adriamycin-induced nephropathy(AIN) in rats.Methods: SD rats were divided into three groups,including normal group,nephropathy model group,group treated with TG.The groups were given adriamycin by tail vein injection except normal group.TG were given in the dose of 50mg/kg by oral once a weeks.24 hours'urines were collected and detected for its protein at the end of 2th、5th and 8th weeks.At the end of 8th weeks,got blood and kidneys.The blood biochemistry parameters were measured by routine methods.The glomerular morphology and podocyte ultrastructure were observed by light microscopy and transmission electron microscopy respectively.The Nephrin and CD2AP expression and distribution change were determined by immunohistochemistry staining.Results: ①Urinary protein: TG could significantly reduce proteinuria in AIN rats.This effect could be seen at week 3 after the treatment and got more prominent at week 6(P〈0.01).②Injuries on podocytes: After treatment with TG for 6 weeks,the injuries on foot processs of podocyte were recovered compared with that in AIN.The effacement of the podocyte foot processes was improved.Most foot processes was restored to normal shape.③Change of slit diaphragm related protein: After treatment with TG for 6 weeks,the expression of nephrin and CD2AP was significantly increased compared with that in AIN rats.The abnormal distribution of Nephrin and CD2AP was corrected.The expression of Nephrin and CD2AP was mostly restored to normal continuous linear expression.Conclusion:TG can obviously reduce quantitation of proteinuria in AIN rats,and repair the damage of podocyte,and ease the foot processes to mix together,and also increase the expression level of Nephrin and CD2AP in kidney glomurulus so as to alleviate chronic inflammation of kidney organization.
Keywords:Nephrotis syndrome/chemically induced Nephrotis syndrome/drug effects Nephrotis syndrome/pathology  
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