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作 者:林章梅 张彩香[1] 梁艳玲[2] 王会中[2] 张鋆歆[2] 李丽[2] 赵蕾[2] 曲建昌[2] 祝开思[1] LIN Zhang-mei ZHANG Cai-xiang LIANG Yan-ling et al(Graduate College of Southern Medical University, Guangzhou 510515, China)
机构地区:[1]南方医科大学研究生学院,广州510515 [2]解放军第305医院内分泌科
出 处:《中国糖尿病杂志》2017年第2期168-172,共5页Chinese Journal of Diabetes
基 金:解放军总参军事医学和老年病科研基金(ZCWS14B12)
摘 要:目的观察α-平滑肌肌动蛋白(α-SMA)及转化生长因子-β1(TGF-β1)在高尿酸血症(HUA)大鼠肾小管间质纤维化(RIF)过程中的表达及意义。方法 SD大鼠36只,随机分为对照组(Con)、模型组及非布司他组,每组12只。氧嗪酸钾(OP)溶于0.5%的羧甲基纤维素钠(CMC)溶液,模型组和非布司他组用OP灌胃,1次/d,制备HUA模型,非布司他组另予非布司他灌胃,Con组仅予等量0.5%(CMC灌胃。于0、4、8周后检测血尿酸(SUA)、血肌酐(Scr)及BUN,收集24 h尿量,检测24 h尿蛋白定量。第0、4、8周末每组随机处死4只大鼠,HE染色及Masson染色观察肾组织病理变化,免疫组织化学法检测α-SMA、TGF-β1的表达。结果实验4周后,与Con组比较,模型组SUA、Scr、BUN升高(P<0.05或P<0.01),TGF-β1、α-SMA表达量增多(P<0.01),肾小管间质发生纤维化。实验8周后,RIF加重;非布司他组RIF较模型组减轻(P<0.01)。结论 HUA诱导肾组织TGF-β1、α-SMA表达量增加;α-SMA及TGF-β1表达增多促进RIF发生。Objective To observe the expression of α-smooth muscle actin(α-SMA) and transforming growth factor-beta(TGF-β1) in hyperuricemia rats with tubulointerstitial and to explore the possible mechanism of renal pro-fibrotic with these two factors.Methods 36 male SD rats were randomly divided into three groups:control group(Con),model group and Febuxostat group,with 12 rats in each group.0.5%sodium carboxymethy cellulose(CMC) solution containing oteracil potassium(OP)was used to establish hyperuricemia model by gastric gavage once per-day.Therapy group was treated with Febuxostat at the same time.Con group was treated with 0.5%CMC only.Serum uric acid(SUA),creatinine(Scr),urea nitrogen(BUN) and 24-hour urinary protein excretion were measured at 0th,4thand8 th week.4 rats were sacrificed randomly at three times in each group.The histological changes of kidneys were observed via HE staining and Masson staining by light microscopy.The expression of TGF-β1 and cr SMA were examined with immunohistochemistry staining.Results Compared with Con group,the value of serum SUA,Scr,BUN in model group were higher at 4^(th) week(P〈0.05),and the expression of TGF-β1and α-SMA were increased significantly(P〈0.01).The renal interstitium injury was seen in model group at the same time,and became aggravation with the progression of the experiment.Febuxostat group has less renal damage versus model group.Conclusion High expression of TGF-β1 and crSMA induced by hyperuricemia may enhance the development of tubulointerstitial fibrosis.
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