黄酮哌酯对前列腺增生模型大鼠的保护作用机制研究 点击下载
论文标题: 黄酮哌酯对前列腺增生模型大鼠的保护作用机制研究
英文标题:
中文摘要: 目的:研究黄酮哌酯对前列腺增生(BPH)模型大鼠的保护作用机制。方法:将大鼠随机分为假手术组、模型组和黄酮哌酯高、低剂量组(80、40 mg/kg),每组8只。除假手术组外,其余各组大鼠通过去势和注射丙酸睾酮复制BPH模型,丙酸睾酮注射1 h后每组大鼠ig相应药物,每日1次,连续4周。末次给药后,考察前列腺指数;采用天狼星红和Masson染色检测前列腺胶原沉积;免疫组化检测前列腺Ⅰ型胶原、纤维连接蛋白(FN)和上皮钙黏着蛋白(E-cadherin)的表达;酶联免疫吸附法检测前列腺组织中超氧化物歧化酶(SOD)、谷胱甘肽过氧化酶(GPx)、丙二醛(MDA)、表皮生长因子(EGF)和血管内皮生长因子(VEGF)的水平;实时荧光定量聚合酶链反应法检测微小RNA21(miR-21)和转化生长因子β1(TGF-β1)水平。结果:与假手术组比较,模型组大鼠前列腺胶原沉积增多,前列腺指数、FN表达、MDA含量和VEGF、EGF、miR-21、TGF-β1水平均升高(P<0.05),E-cadherin表达、SOD和GPx活力均降低(P<0.05)。与模型组比较,黄酮哌酯高、低剂量组大鼠前列腺胶原沉积减少,前列腺指数、FN表达、MDA含量和VEGF、EGF、miR-21、TGF-β1水平均降低(P<0.05),E-cadherin表达、SOD和GPx活力均升高(P<0.05)。结论:黄酮哌酯抗BPH的机制可能与下调miR-21和TGF-β1表达,抑制氧化应激和血管生成,改善上皮-间质转化有关。
英文摘要: OBJECTIVE: To study the protective mechanism of flavoxate on prostatic hyperplasia in model rats. METHODS: The rats were randomly divided into sham operation group, model group and flavoxate high-dose and low-dose groups (80, 40   mg/kg), with 8 rats in each group. Except for sham operation group, those groups were emasculated and given sterandryl to induce BPH model. They were given relevant medicine intragastrically 1 h after administration of sterandryl, once a day, for consecutive 4 weeks. Sirius red and Masson staining were used to detect the precipitation of collagen in prostate; immunohistochemistry was used to detect the expressions of prostatic type Ⅰ collagen, FN and E-cadherin; ELISA assay was used to determine the levels of SOD, GPx, MDA, EGF and VEGF in prostate. qPCR assay was used to detect the levels of miR-21 and TGF-β1. RESULTS: Compared with the sham operation group, the prostatic collagen was accumulated; prostatic index, the expression of FN, MDA content and levels of VEGF, EGF, miR-21 and TGF-β1 were increased (P<0.05); the expression of E-cadherin, and the activity of SOD and GPx were decreased (P<0.05). Compared with model group, the precipitation of prostatic collagen was decreased; prostatic index, the expression of FN, MDA content, the levels of VEGF, EGF, miR-21 and TGF-β1 were decreased in flavoxate high-dose and low-dose groups (P<0.05); while the expression of E-cadherin and the activity of SOD and GPx were increased (P<0.05). CONCLUSIONS: Flavoxate can inhibit BPH, the mechanism of which may associated with down-regulating the expressions of miR-21 and TGF-β1, inhibiting oxidative stress and angiogenesis and improving epithelial-mesenchymal transition.
期刊: 2016年第27卷第31期
作者: 杜丽芬,陈镜楼
英文作者: DU Lifen,CHEN Jinglou
关键字: 黄酮哌酯;前列腺增生;氧化应激;血管生成;上皮-间质转化;大鼠
KEYWORDS: Flavoxate; Benign prostatic hyperplasia; Oxidative stress; Angiogenesis; Epithelial-mesenchymal transition; Rats
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