摘要
目的观察肾疏宁对肾小管间质损害大鼠TGF-β1、CTGF蛋白及CTGFmRNA表达的影响。方法在系膜增生性肾炎(MsPGN)模型基础上,延长造模时间至12～16周,使其自然发展成肾小管间质损害模型,观察肾疏宁对肾小管间质TGF-β1、CTGF蛋白及CTGFmRNA表达的影响,并设苯那普利为阳性对照组。结果第12～16周末,造模各组肾小管间质TGF-β1、CTGF蛋白及CTGFmRNA表达量均明显高于正常组(P<0.01),肾疏宁组、苯那普利组均显著低于模型组(P<0.01);第12周末,肾疏宁组与苯那普利组比较无显著性差异(P>0.05),而第16周末,肾疏宁组明显低于苯那普利组(P<0.01)。结论肾疏宁可对抗CTGF基因的表达,直接或间接抑制TGF-β1,从而保护肾小管间质损害。
Objective To observe the effect of ＂Shen Shu Ning＂ on transforming growth factor-beta-1 （TGF-β1） and connective tissue growth factor （CTGF） in the animal model of progressive tubulointerstitial injury （TII）. Methods Make the model of mesangial proliferative glomerulonephritis （MsPGN） rats and extend the time of the model to 12th-16th weeks and make the model naturally develop to tubulointerstitial lesion model. Using the model of progressive TII,we observed the effect of ＂Shen Shu Ning＂（SSN） on TGF-β1and CTGF. At the same time,use benazepril as control. Results Untreated rats had a significant increase in the levels of tubulointerstitial protein for TGF-＇beta and CTGF and CTGF mRNA （P〈 0.01）,SSN and benazepril could decrease the levels of tubulointerstitial protein for TGF-beta and CTGF and CTGF mRNA （P〈 0.01） during 12th -16th weeks. The curative effects of SSN is the same as benazepril in the 12th week（P〉0.05）,but SSN exhibited a distinct advantage over benazepril in THE 16th week（P〈0.01）. Conclusion SSN can antagonize CTGF expression and directly or indirectly restrain the effect of TGF-beta,and protect tubulointerstitial lesions.
出处
《上海中医药杂志》
北大核心
2006年第6期59-61,共3页
Shanghai Journal of Traditional Chinese Medicine
基金
天津市自然科学基金资助项目(023611511)
关键词
肾疏宁
系膜增生性肾炎
肾小管间质
转化生长因子-β1
结缔组织生长因子
＂Shen Shu Ning＂
tubulointerstitial lesions
mesangial proliferative glomerulonephritis
connective tissue growth factor
transforming growth factor-betal
