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作 者:赵爱青[1] 张晓明[1] 侯恒[1] 李荣山[2] 马存根[1]
机构地区:[1]大同大学医学院内科教研室,山西大同037008 [2]山西医科大学第二临床医学院肾内科,山西太原030001
出 处:《中国中医药信息杂志》2007年第8期36-38,共3页Chinese Journal of Information on Traditional Chinese Medicine
基 金:山西省自然科学基金资助项目(20021120)
摘 要:目的观察姜黄素对单侧输尿管梗阻(UUO)大鼠肾间质纤维化的影响,并与依那普利进行比较。方法采用UUO致肾间质纤维化大鼠模型,术后第4周处死各组大鼠,用HE、Masson染色评定肾小管间质纤维化程度;用免疫组化方法检测肾组织内转化生长因子β1(TGF-β1)、结缔组织生长因子(CTGF)和基质金属蛋白酶抑制剂-1(TIMP-1)的表达部位及蛋白表达水平。结果与假手术组相比,模型组大鼠肾间质纤维组织面积显著扩大(P<0.01),肾组织内TGF-β1、CTGF和TIMP-1蛋白质表达均显著上调(P<0.01)。姜黄素或依那普利干预后,上述上调指标都被显著抑制(P<0.05或P<0.01)。两种药物作用比较无显著差异(P>0.05)。结论姜黄素或依那普利对UUO大鼠的干预效果相似,此可能与下调肾组织内TGF-β1和CTGF,进而部分抑制TIMP-1的表达有关。Objective To investigate the effect of curcumin on renal interstitial fibrosis following unilateral ureteral obstruction (UUO), and compare the effects of Curcumin with that of Enalapril. UUO rat model was used. Male Wistar rats were randomly divided into four groups with 8 rats each- shame-operated group (0.9% saline solution), model group (dimethyl sulphoxide, DMSO), Curcumin treatment group [curcumin 100 mg/(kg · d)], and Enalapril treatment group [enalaprfl 10 mg/(kg · d)]. All rats were killed 4 w after surgery. The degree of tubulointerstitial fibrosis was scored by HE and Masson staining. The sites and levels of protein expression of TGF-β1, CTGF and TIMP-1 were detected by immunohistochemistry staining. Result Compared with those of shame-operated group, the blood urea nitrogen level was significantly increased (P〈0.01); and the relative area of interstitial fibrosis was also significantly enlarged, the expression of TGF-β1. CTGF and TIMP-1 protein was significantly up-regulated in kidney tissue of model group (P〈0.01). After intervention with Curcumin or Enalapril, the upregulation of the above-mentioned parameters were all significantly inhibited (P〈0.05 or P〈0.01). There was no significant difference of intervention effects between Curcumin and Enalapril (P〉0.05). Conclusion Pharmacological effects of Curcumin or Enalapril on unilateral ureteral obstruction rats are quite similar. These effects may result from the down-regulation of TGF-β1, CTGF and TIMP-1 expression in kidney tissue.
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