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作 者:高红宇[1] 邵菊芳[1] 何晓峰[1] 易艳[1] 黄晓丽[1] 刘晓城[1]
机构地区:[1]华中科技大学同济医学院附属同济医院肾病科,湖北武汉430030
出 处:《中国现代医学杂志》2006年第20期3094-3097,3100,共5页China Journal of Modern Medicine
摘 要:目的探讨苦参素对单侧输尿管梗阻(UUO)大鼠肾小管上皮细胞转分化的影响及可能机制。方法雄性SD大鼠随机分为3组:假手术组,单侧输尿管结扎(UUO)组,治疗组。治疗组在UUO的基础上每天以苦参素100mg/Kg腹腔注射。各组于术后第7,14及21天分别处死5只大鼠。用PAS及Masson染色法观察肾脏病理改变。用免疫组织化学法检测转化生长因子β1(TGF-β1),Smad3及α-平滑肌肌动蛋白(α-SMA)的表达。结果与UUO组相比,治疗组梗阻侧肾脏TGF-β1、Smad3和α-SMA的表达明显减少,肾小管损害和肾间质纤维化的程度也明显减轻。结论苦参素可下调TGF-β1的表达,抑制肾小管上皮细胞转分化及肌成纤维细胞的活化与增殖,其作用途径可能是通过下调Smad3的表达,从而干预Smad3介导的细胞内信号转导。[Objective] To study the effect and mechanisms of Kushenin on the process of tubular epithelial-mecenchymal transformation following unilateral ureteral obstruction in rats. [Methods] Sprague-Dawley male rats were randomly assigned to 3 groups: sham operation group, UUO group, treatment group. The rats of treatment group were treated with daily intraperitoneally injection of 100 mg/kg of kushenin after operation. Five rats of each group were killed respectively at 7, 14, 21 days after operation. Renal tissue hisological changes were observed by PAS and Masson stain. Immunohistochemistry was performed to investigate the expression of TGF-β1, Smad3 and α- SMA in kidney. [Results] Compared to UUO group, the expression of TGF-β1, Smad3 and α-SMA was decreased significantly in treatment group and the degree of tubular damage and interstitial fibrosis was also ameliorated. [Conclusion] Kushenin could inhibit tubular epithelial-mesenehymal transformation (EMT), suppress the activation and proliferation of myofibroblast by downregulating the expression of TGF-β1. The probable mechanism was to intervene with the TGF-β1/Smad3 signal pathway by downregulating, the expression of Smad3.
关 键 词:苦参素 肾间质纤维化TGF—β1 SMAD3
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