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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。
Objective To observe the effect of “Shenshu Ⅱ” on renal function, pathology, podocyte number and Notch-P53 signaling pathway in focal segmental glomerulosclerosis (FSGS) rats. Methods SD rats were induced by left nephrectomy and doxorubicin injection. FSGS rats were randomly divided into three groups according to body weight: model group, benazepril group and Shen-Su-Ⅱ group, with 12 rats in each group. (12). The patients in benazepril group were treated with benazepril [9.25 mg / (kg · d)], and those with nephrotoxicity were treated with nephrotic syndrome (9.71 g / (kg · d)]. In the control group, Saline, were continuous gavage for 12 weeks. Serum creatinine (SCr), serum urea nitrogen (BUN), high density lipoprotein (HDL) and apolipoprotein A1 (Apo-A1) levels were determined. The changes of glomerular sclerosis, number of podocytes, Notch1, Hes-1, P53 and Bad protein expression in key sites of Notch-P53 apoptotic pathway were observed. Results Compared with the model group, the levels of HDL increased significantly at 4, 8 and 12 weeks in benazepril group and Shen-Su-Ⅱ group (P <0.05). At 8 and 12 weeks, SCr decreased significantly (P <0.05) -A1 significantly increased (P <0.05). After 12 weeks of treatment, BUN, glomerular sclerosis index, relative area of glomerular mesangial matrix, Notch1, Hes-1, P53, The number of cells increased significantly (P <0.05). Conclusion Shenshu Ⅱ may inhibit the process of podocyte apoptosis by regulating Notch-P53 pathway, and then delay the progression of the disease in FSGS rats.