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作 者:宋纯东[1] 杨晓丽 薛黎明[3] 任瑞英[4] 侯小静[5]
机构地区:[1]河南中医学院第一附属医院,河南郑州450008 [2]郑州市金水区人民医院,河南郑州450000 [3]河南中医学院第三附属医院,河南郑州市450003 [4]郑州市儿童医院,河南郑州450005 [5]河南中医学院,河南郑州450003
出 处:《广州中医药大学学报》2012年第6期691-694,698,共5页Journal of Guangzhou University of Traditional Chinese Medicine
基 金:河南省科技厅科技攻关资助项目(编号:0412002100)
摘 要:【目的】探讨益肾活血方对糖尿病肾病(DN)大鼠肾组织中转化因子-β1/p38丝裂原活化蛋白激酶(TGF-β1/p38MAPK)表达的影响。【方法】选用SD大鼠,随机分为正常组、模型组、治疗组(给予19.5 g.kg-1.d-1的益肾活血方药液灌胃),采用链脲佐菌素(55 mg/kg)一次性腹腔注射复制DN模型。采用全自动生化分析仪检测各组大鼠24 h尿蛋白、血肌酐(Scr)、尿素氮(BUN)、血清白蛋白(ALB)、血糖水平;Leica Qwin Plus图像分析系统测量肾小球直径、肾小管短径和完整肾小管数目,并称取各组大鼠左肾质量、计算肥大指数;过碘酸雪夫反应(PAS)染色观察各组大鼠肾组织病理变化;免疫组织化学法检测肾组织TGF-β1、p38MAPK表达。【结果】治疗组能够降低模型大鼠肾组织TGF-β1、p38MAPK的表达及24 h尿蛋白、Scr、BUN、血糖水平,升高ALB水平,缩小肾小球直径及肾小管短径,增加完整肾小管数量,改善肾组织病理变化,降低肾质量及肥大指数,与模型组比较差异均有统计学意义(P<0.05或P<0.01)。【结论】益肾活血方可能通过影响DN大鼠肾组织TGF-β1/p38MAPK的表达而改善上述生化指标,减轻肾脏病理损害。Objective To investigate the influence of Yishen Huoxue Recipe (YHR), a Chinese herbal prescription with the actions of tonifying kidney and activating blood, on the renal transforming growth factor beta 1/p38 mitogen-activated protein kinase (TGF-β1/p38MAPK) expression levels in rats with diabetic nephropathy (DN). Methods SD rats were randomized into normal group, model group, and YHR group (in the dose of 19.5g·k^-1·d^-1). DN rat model was induced by one-dose intraperitoneal injection of 55 mg/kg of streptozocin.Automatic biochemical analyzer was used to detect 24-hour urinary protein, serum creatinine (SCr), blood urea nitrogen (BUN), plasma albumin (ALB), blood glucose level of the experimental rats, and Leica Qwin Plus image analysis system was used for the measurement of glomerular diameter, tubular short diameter and the number of complete tubular. The weight of rat left kidney was measured to calculate the hypertrophy index. Rat renal pathology was observed after periodic acid-Schiff staining, and renal TGF-β1 and p38MAPK expression levels were detected with immunohistochemal assay. Results After treatment, TGF-β1 and p38MAPK expression levels, 24-h urinary protein, Scr, BUN, and blood glucose were decreased, ALB was increased, glomerular diameter and tubular short diameter were shortened, the number of complete tubular was increased, renal pathology was improved, and kidney weight and hypertrophy index with the model group ). Conclusion YHR can pathological injury through the regulation of TGF-β1 were reduced in YHR group (P 〈0.05 or P 〈0. 01 compared improve the biochemical parameters and relieve the renal and p38MAPK expression.
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