摘要
目的 :探讨雷公藤多甙片 (GTT)治疗IgA肾病的分子机理。方法 :制造IgA肾病小鼠模型。HE染色光镜下观察肾小球系膜增殖 ;原位末端标记法 (TUNEL)检测系膜区凋亡细胞 ;免疫组化法观察系膜区Fas、PCNA的表达。结果 :GTT治疗组肾小球系膜区凋亡率较模型组升高 (P <0 .0 1) ,Fas表达增强 (P <0 .0 5 ) ,PCNA表达下降 (P <0 .0 1) ,病理损害减轻。结论 :GTT可能通过调控系膜区Fas的表达 ,诱导IgA肾病系膜区细胞凋亡 ,进而抑制系膜增殖。
Purpose: To study the molecular mechanism of Glucosidorum Tripterygll Totorum(GTT) in treating IgA nephropathy. Method: IgA nephropathy rats were modeled to observe the mesentery proliferation under the stained glass. The depressed and dead cells were tested with orthotopic end label method, and the Fas,PCNA reaction of mesentery area of the treated group was higher than that of the model group(P<0,01), with the Fas reaction strengthened (P<0.05),the PCNA reaction decreased (P<0.01) and the pathological damage lightened. Conclusion: GTT may make the IgA nephropathy mesentery cell depressed and dead by regulating the Fas reaction of the mesentery area , thus to inhibit the mesentery proliferation.
出处
《河南中医》
2004年第7期26-28,共3页
Henan Traditional Chinese Medicine
基金
国家中医药管理局科技攻关项目 [2 0 0 0-J- 2(PMQB) 387]
关键词
雷公藤多甙片
IGA肾病
细胞凋亡
基因
Glucosidorum Tripterygll Totorum
IgA nephropathy
cell depression and death
gene