中文摘要：

目的观察肾苏Ⅱ方对局灶节段性肾小球硬化（focal segmental glomerulosclerosis,FSGS）大鼠肾脏功能、病理、足细胞数量、Notch-P53凋亡通路标志蛋白的影响。方法采用左肾切除加阿霉素注射法诱发SD大鼠FSGS模型,依体重随机分为3组,模型组、贝那普利组和肾苏Ⅱ方组,每组12只,另设对照组（12只）。贝那普利组予贝那普利[9.25 mg/（kg·d）]、肾苏Ⅱ方组予肾苏Ⅱ方[9.71 g/（kg·d）],对照组、模型组予等量生理盐水,均连续灌胃12周。检测大鼠肌酐（serum creatinine,SCr）、血清尿素氮（blood urine nitrogen,BUN）、高密度脂蛋白（high density lipoprotein,HDL）、载脂蛋白A1（apolipoprotein-A1,Apo-A1）水平。观察肾小球硬化改变、足细胞数量分析、Notch-P53凋亡通路关键位点的Notch1、Hes-1、P53及Bad蛋白表达。结果与模型组比较,贝那普利组和肾苏Ⅱ方组治疗4、8、12周,HDL明显上升（P〈0.05）;治疗8、12周,SCr明显下降（P〈0.05）、Apo-A1明显上升（P〈0.05）;治疗12周,BUN、肾小球硬化指数、肾小球系膜基质相对面积、Notch1、Hes-1、P53、Bad蛋白明显减少（P〈0.05）,足细胞数量明显增加（P〈0.05）。结论肾苏Ⅱ方可能通过调控Notch-P53通路,阻抑足细胞凋亡进程,进而延缓FSGS大鼠疾病进展。

英文摘要：

Objective To observe the effects of Shensu Ⅱ Recipe（ SⅡ R） on renal function,pathology,the number of podocytes,and key positions of Notch-P53 apoptosis pathway in rats with focal segmental glomerulosclerosis（ FSGS）.Methods FSGS model was induced in SD rats by injecting Adriamycin and left nephrectomy. They were randomly divided into the model group,the Benazepril group,and the SⅡ R group according to body weight,12 in each group. Besides,another 12 rats was recruited as the control group. Benazepril [9. 25 mg/（ kg·d） ]and SⅡ R [9. 71 g/（ kg·d） ]were respectively given to rats in the Benazepril group and the SⅡ R group by gastrogavage. Equal volume of normal saline was respectively given to rats in the control group and the model group by gastrogavage. All medication lasted for 12 weeks. Levels of serum creatinine（ SCr）,blood urine nitrogen（ BUN）,high density lipoprotein（ HDL）,apolipoprotein-A1（ Apo-A1） were detected. The changes of glomerulosclerosis were observed. The number of podocyte,the protein expressions of Notch1,Hes-1,P53,and Bad were also determined. Results Compared with the model group,HDL significantly increased after 4-,8-,and 12-week treatment（P〈0. 05）; SCr significantly decreased（P〈0. 05） and Apo-A1 significantly increased（P〈0. 05） after8-and 12-week treatment; BUN,glomerulosclerosis index,the relative area of glomerular mesangial matrix,Notch1,Hes-1,P53,and Bad protein significantly decreased（P〈0. 05）,and the number of podocytes significantly increased（P〈0. 05） after 12-week treatment in the rest two groups. Conclusion SⅡ R postponed the development of FSGS rats possibly through regulating notch-P53 signaling pathway and inhibiting apoptosis process of podocytes.