肾疏宁对肾小管间质损害大鼠表型转化的影响

The effect of herbal medicine of Shen Shu Ning on phenotype transdifferentiation in tubulointerstitial injury rats

目的:观察肾疏宁对肾小管间质损害大鼠表型转化的影响。方法:在系膜增生性肾炎模型基础上,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α-SMA、PCNA、CD68蛋白表达的影响,并设苯那普利为阳性对照组。结果:12～16周末,造模各组肾小管间质-α平滑肌肌动蛋白(-αSMA)、增殖细胞核抗原(PCNA)、CD68蛋白表达量均明显高于正常组(P<0.05或P<0.01)。第12周末,治疗组均能降低肾小管间质α-SMA、CD68表达量(均P<0.01),但对肾小管PCNA表达量影响不明显,而对间质PCNA表达量具有明显的降低作用(均P<0.01)。第16周末,肾疏宁组明显优于苯那普利组(均P<0.01)。结论:肾疏宁对肾小管间质损害具有明显的保护作用,其机制可能是通过抑制炎细胞浸润,抑制间质细胞的增殖,逆转肾小管间质的表型转化而实现的。

Objective： To observe the effect of Shen Shu Ning （SSN） on phenotype transdifferentiation in the animal model of progressive tubulointerstitial injury（TII）. Methods： The model of Mesangial proliferative glomerulonephritis （MsPGN） in rat was made. After 12^th-16^th weeks, the model naturally developed to tubulointerstitial lesion model. Using the model of progressive TII, we observed the effect of herbal medicine of SSN through expressed protein of α-smooth muscle actin （α-SMA）, proliferating cell nuclear antigen（PCNA） and monocyte/macrophage（CD68^＋）. At the same time, benazepril was used as control. Resuits： Untreated rats had a significant increase in the levels of α-SMA,PCNA,CD68 in tubulointerstitium at end of 12^th-16^th weeks （P〈0.05 or P〈0.01）. At the end of 12^th weeks, SSN and benazepril could decrease the levels of α-SMA and CD68 （P〈0.01） in tubulointerstitium, and decrease the levels of PCNA in interstitium （P〈0.01）, but not in canaliculi .At the end of 16^th weeks, SSN exhibited a distinct advantage over benazepril （P〈0.01）. Conclusion： SSN has distinct effects of protecting tubulointerstitial lesions. SSN could inhibit the infiltration of inflammatory cell, proliferation of interstitial cell, and reverse tubulointerstitial phenotype transdifferentiation.