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目的:观察20(S)原人参二醇[20(S)-PPD]对阿霉素肾病大鼠的肾脏保护作用并探讨机制。方法:30只SD大鼠随机分为三组:正常对照组、阿霉素组和20(S)-PPD组(干预组)。阿霉素组和干预组分别阴茎静脉注射阿霉素7.5mg/kg,正常对照组注射等剂量的生理盐水,造模后干预组随即20(S)-PPD灌胃8周[200mg/(kg.d)],实验结束留取大鼠血、尿及肾脏组织,分别检测各组血、尿生化指标,常规染色观察肾脏组织学改变、电镜观察足细胞损伤情况及免疫组化染色观察肾小管间质纤维化的程度。结果:(1)生化指标:阿霉素组尿白蛋白,尿白蛋白/肌酐比、血尿素氮、三酰甘油、胆固醇均较正常对照组明显升高,血白蛋白较正常对照组明显降低,干预组各项指标均较阿霉素组明显好转,差异均具有统计学意义;(2)组织学改变:阿霉素肾病大鼠肾小球可见明显的局灶节段性硬化改变,可见肾小管扩张、炎细胞浸润及间质纤维化等改变,而干预组较阿霉素组肾小球及肾小管损伤均明显减轻;(3)电镜结果:阿霉素肾病大鼠肾小球足细胞足突弥漫性融合,可见部分足细胞脱落及裸露的基膜,干预组较阿霉素组足细胞损伤明显减轻;(4)免疫组化:阿霉素组α平滑肌肌动蛋白、I型胶原及纤维连接蛋白各项指标表达较正常对照组明显上调,干预组较阿霉素组表达量显著下降,差异具有统计学意义。结论:20(S)-PPD对阿霉素肾病大鼠的肾脏具有明显的保护作用,其机制可能与保护足细胞损伤,减少尿蛋白,进而缓解肾小管间质损害有关。
Objective: To observe the protective effects of 20 (S) protopanaxadiol [20 (S) -PPD] on adriamycin-induced nephropathy in rats and its mechanism. Methods: Thirty SD rats were randomly divided into three groups: normal control group, doxorubicin group and 20 (S) -PPD group (intervention group). Doxorubicin group and intervention group were given doxorubicin 7.5mg / kg intravenously, the normal control group were injected with the same dose of normal saline, and the intervention group was given 20 (S) -PPD for 8 weeks [200mg / (kg .d)]. At the end of the experiment, blood, urine and kidney tissues were collected from rats. The biochemical indexes of blood and urine in each group were detected. The histological changes of kidney were observed by routine staining. The damage of podocytes was observed with electron microscope. The degree of interstitial fibrosis. Results: (1) Biochemical index: Compared with normal control group, urinary albumin, urinary albumin / creatinine ratio, blood urea nitrogen, triglyceride and cholesterol in adriamycin group were significantly higher than those in normal control group , The intervention group indicators were significantly improved compared with doxorubicin group, the differences were statistically significant; (2) histological changes: Adriamycin nephrosis rats showed significant focal segmental sclerosis changes can be seen Tubular dilatation, inflammatory cell infiltration and interstitial fibrosis and other changes, while the intervention group than doxorubicin group glomerular and tubular damage were significantly reduced; (3) electron microscopy results: doxorubicin nephropathy rat glomerular foot Cell foot process diffuse fusion, showing part of the podocyte shedding and bare basement membrane, intervention group than doxorubicin group podocyte injury was significantly reduced; (4) Immunohistochemistry: Adriamycin group α smooth muscle actin, type I The expression of collagen and fibronectin were significantly up-regulated compared with the normal control group. The expression of collagen and fibronectin in the intervention group was significantly lower than that in the doxorubicin group. The difference was statistically significant. CONCLUSION: 20 (S) -PPD has a significant protective effect on the kidneys of adriamycin-induced nephropathy rats. The mechanism may be related to the protection of podocyte injury, the decrease of urinary protein and the alleviation of tubulointerstitial damage.