丹参酮I通过激活Nrf2-ARE通路阻抑放射性膀胱炎早期损伤的形成  被引量:5

Tanshinone I inhibits radiation-induced bladder injury by activating Nrf2-ARE signaling pathway

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作  者:彭昆 高文强[3] 邱雪峰[1,2] 陈蔚[1,2] 张士伟 郭宏骞[1,2] PENG Kun;GAO Wen -qiang;QIU Xue- feng;CHEN Wei;ZHANG Shi -wei;GUO Hong -qian(Department of Urology,Drum Tower Hospital Affiliated to Medical School of Nanjing University,Nanjing 2100081;Institute of Urology,Nanjing University,Nanjing 210008;Medical School of Southeast Uni versity,Nanjing 210009,China)

机构地区:[1]南京大学医学院附属鼓楼医院泌尿外科,江苏南京210008 [2]南京大学泌尿外科学研究所,江苏南京210008 [3]东南大学医学院,江苏南京210009

出  处:《现代泌尿外科杂志》2018年第7期533-538,552,共7页Journal of Modern Urology

基  金:南京市卫生局重点项目(No.ZKX16035);江苏省自然科学基金青年基金(No.BK20150112);南京市杰出青年基金项目(No.JQX16025)

摘  要:目的验证丹参酮I(T-1)是否通过Nrf2-ARE通路的激活阻抑膀胱接受射线后早期放射性损伤的形成。方法将人永生化尿路上皮细胞(SV-HUC-1)分为对照组(Control),T-1处理组(T-1),X-射线照射组(X-ray),T-1治疗组(X-ray+T-1)。使用cck-8试剂盒及DCFH-DA活性氧试剂盒比较各组细胞损伤情况。通过Western-Blot法测定各组细胞总蛋白中Nrf2-ARE信号通路的变化。雌性6周龄美国费城癌症研究所小鼠(ICR小鼠)被随机分为对照组(Control),T-1处理组(T-1),X-射线照射组(X-ray),T-1治疗组(X-ray+T-1)。每组小鼠预处理10d后实验组予以盆腔放射。照射3d及1周后比较各组膀胱组织Nrf2-ARE信号通路蛋白表达量。测量膀胱黏膜厚度及组织内SOD变化水平。结果在体外实验中,T-I治疗组与X-射线照射组对比,细胞活力较高同时活性氧水平较低(P<0.05)。T-1治疗组中Nrf2-ARE信号通路相关蛋白表达量高于X-射线处理组(P<0.05)。在体内实验中T-1治疗组与X-射线照射组相比,膀胱黏膜厚度更小同时SOD水平较高(P<0.05)。T-1治疗组总蛋白中Nrf2-ARE信号通路相关蛋白表达量高于X-射线处理组。结论 T-1对于放射性膀胱损伤具有保护作用,Nrf2信号通路的激活在其中可能发挥了重要作用。Objective To investigate the role of Nrf2-ARE signaling pathway in tanshinone I(T-1)alleviating radiationinduced bladder injury.Methods Human uroepithelial cell line(SV-HUC-1)was randomly divided into 4 groups:control group(Control),T-1 group(T-1),X-ray group(X-ray),and X-ray+T-1 group(X-ray+T-1).Cell viability,reactive oxygen species(ROS)and expression of Nrf2-ARE signaling pathway were compared among all groups using CCK-8 kit,DCFH-DA kit and Western blot respectively.Female ICR mice were randomly allocated into 4 groups:control group(Control),T-1 group(T-1),X-ray group(X-ray),X-ray+T-1 group(X-ray+T-1).Mice in X-ray group and X-ray+T-1 group were exposed to radiation.Mice in T-1 group as well as in X-ray+T-1 group were treated with T-1.Bladder samples were collected3 days and7 days after radiation.Histology,superoxideismutase(SOD)and expression of Nrf2-ARE signaling pathway were compared among all groups.Results In vitro,T-I treatment increased the cell viability,lowered the ROS level,and improved the levels of Nrf2,GCLC,NQO1,and GPX2 in X-ray+T-I group than in X-ray group(P〈0.05).In vivo,T-I treatment decreased the mocusa thickness,increased the level of SOD,and improved the levels of Nrf2,GCLC,NQO1,and HEMOX1 in X-ray+T-I group than in X-ray group(P〈0.05).Conclusion T-1 may have protective effect against radiation-induced bladder injury by activating Nrf2 signaling pathway.

关 键 词:放疗 膀胱 放射性膀胱损伤 丹参酮Ⅰ 氧化应激 NRF2 

分 类 号:R694.3[医药卫生—泌尿科学]

 

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