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目的:观察肾疏宁对肾小管间质损害大鼠FN、ColⅢ、PAI-1mRNA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FN、ColⅢ、PAI-1mRNA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FN、ColⅢ、PAI-1mRNA表达量均明显升高(P<0.05或P<0.01),肾疏宁组、苯那普利组均显著低于模型组(P<0.05或P<0.01),第12周末,肾疏宁组与苯那普利组比较无统计学差异(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:肾疏宁能抑制细胞外基质的合成,促进其降解,从而保护肾小管间质损害。
Objective: To observe the effect of Shenshuning on the expression of FN, Col III and PAI-1 mRNA in rats with tubulointerstitial damage. METHODS: On the basis of the mesangial proliferative nephritis (MsPGN) model, the prolonged modelling time was extended to 12 to 16 weeks, which allowed it to spontaneously develop a tubular interstitial damage model. The observation was made that the kidney sulphonation was performed on the tubulointerstitial FN, Col III, The effect of PAI-1 mRNA expression was determined and Benazepril was set as a positive control group. Results: At the end of the 12th to the 16th week, the expression of FN, Col III, and PAI-1 mRNA in the renal tubulointerstitium increased significantly (P<0.05 or P<0.01). Both the kidney-shuning group and benazepril group were Significantly lower than the model group (P<0.05 or P<0.01). At the end of the 12th week, there was no statistical difference between the Shenshuning group and benazepril group (P>0.05), but at the end of the 16th week, the kidney Shuning group was significantly It was lower than the Benazepril group (P<0.01). Conclusion: Shenshuning can inhibit the synthesis of extracellular matrix and promote its degradation, thus protecting renal tubulointerstitial damage.