虎杖苷对肾纤维化模型大鼠肾组织中MMP-9和TIMP-1蛋白表达的影响
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篇名: 虎杖苷对肾纤维化模型大鼠肾组织中MMP-9和TIMP-1蛋白表达的影响
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摘要: 目的:考察虎杖苷对肾纤维化模型大鼠肾组织中基质金属蛋白酶9(MMP-9)和基质金属蛋白酶组织抑制物1(TIMP-1)蛋白表达的影响,探讨其延缓大鼠肾纤维化的作用机制。方法:将40只大鼠随机分为假手术组(生理盐水)、模型组(生理盐水)、虎杖苷组(100 mg/kg)和贝那普利组(阳性对照,5 mg/kg)。除假手术组外,其余各组大鼠均采用单侧输尿管梗阻法制备肾纤维化大鼠模型。术后1 h,各组大鼠灌胃相应药物,每天给药1次。连续给药4周后,检测各组大鼠尿液中β2微球蛋白(β2-MG)、N-乙酰-β-D-氨基葡萄糖苷酶(NAG)含量和血清中尿素氮(BUN)、肌酐(Cr)含量;苏木素-伊红染色观察大鼠肾组织病理改变,并进行评分;免疫组织化学法检测大鼠肾组织中MMP-9和TIMP-1蛋白表达。结果:与假手术组比较,模型组大鼠尿液中β2-MG、NAG含量和血清中BUN、Cr含量均显著升高(P<0.05),并且大鼠肾组织的病理评分和组织中MMP-9、TIMP-1蛋白的表达水平也显著升高(P<0.01)。与模型组比较,虎杖苷组和贝那普利组大鼠肾组织中MMP-9蛋白表达水平持续增高(P<0.01),其余各指标水平均显著降低(P<0.05或P<0.01);且虎杖苷组与贝那普利组比较大鼠各指标水平差异均无统计学意义(P>0.05)。结论:虎杖苷延缓大鼠肾纤维化进程的机制可能与上调大鼠肾组织中MMP-9蛋白表达和下调TIMP-1蛋白表达,升高MMP-9/TIMP-1的比值有关。
ABSTRACT: OBJECTIVE: To investigate the effects of polydatin on protein expression of MMP-9 and TIMP-1 in renal tissue of renal fibrosis model rats, and to investigate the mechanism of delaying renal fibrosis in rats. METHODS: A total of 40 rats were randomly divided into sham operation group (normal saline), model group (normal saline), polydatin group (100 mg/kg) and benazepril group (positive control, 5 mg/kg). Except for sham operation group, renal fibrosis rat model was induced by unilateral ureteral obstruction in other groups. 1 h after surgery, each group was given relevant medicine intragastrically, once a day. After 4 weeks of consecutive treatment, the contents of β2-microglobulin (β2-MG) and N-acetyl-β-D-glucosaminidase (NAG) in urine, serum contents of BUN and Cr were detected in each group. HE staining was used to observe and score pathological changes of renal tissue in rats. Protein expressions of MMP-9 and TIMP-1 in renal tissue of rats were determined by immunohistochemistry. RESULTS: Compared with sham operation group, the contents of β2-MG and NAG in urine, serum contents of BUN and Cr were increased significantly in model group (P<0.05), and pathological score and protein expressions of MMP-9 and TIMP-1 were also increased significantly (P<0.01). Compared with model group, protein expression of MMP-9 in renal tissue were increased continuously in polydatin group and benazepril group (P<0.01); other indexes were decreased significantly (P<0.05 or P<0.01), and there was no statistical significance in each index between polydatin group and benazepril group (P>0.05). CONCLUSIONS: Polydatin can delay renal fibrosis, the mechanism of which may be associated with up-regulating protein expression of MMP-9, down-regulating protein expression of TIMP-1 and increasing the ratio of MMP-9/TIMP-1.
期刊: 2018年第29卷第7期
作者: 王松,赵晓玉,梁艳,张英杰,齐跃东
AUTHORS: WANG Song,ZHAO Xiaoyu,LIANG Yan,ZHANG Yingjie,QI Yuedong
关键字: 虎杖苷;肾纤维化;单侧输尿管梗阻;基质金属蛋白酶9;基质金属蛋白酶组织抑制物1
KEYWORDS: Polydatin; Renal fibrosis; Unilateral ureteral obstruction; MMP-9; TIMP-1
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