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作 者:吴松 李怡 陈惠宇 杜亚琴 张萍 汪伟 李贵森 王莉 丁涵露 WU Song;LI Yi;CHEN Hui-yu;DU Ya-qin;ZHANG Ping;WANG Wei;LI Gui-sen;WANG Li;DING Han-lu(Medical Colle^+e$Electronic Science and Technology University$Chengdu 610072$C2%a;Department of Nephrology$Sichuan Academy of Medical Sciences&Sichuan Provincial Peopled Hospital$Chengdu 610072$Chia)
机构地区:[1]电子科技大学医学院,四川成都610072 [2]四川省医学科学院.四川省人民医院肾内科,四川成都610072
出 处:《实用医院临床杂志》2018年第2期1-3,共3页Practical Journal of Clinical Medicine
基 金:国家自然科学基金资助项目(编号:81170680)
摘 要:目的探讨肝X受体(LXR)激动剂T0901317对db/db小鼠肾脏肝X受体表达水平及其活性的影响。方法将8周龄雄性db/db小鼠分为db/db组和db/db+T0901317组(均n=7),同时以同龄同性别野生型C57BL/6小鼠为对照组(n=7)。对照组和db/db组小鼠胃饲生理盐水(50μl/只/天×7),db/db+T0901317组小鼠胃饲T0901317[12.5 mg/(kg·d)×7];4周后RT-PCR检测肾组织ABCA1 mRNA水平;Western blot检测上述各组小鼠肾组织LXRα、LXRβ蛋白表达水平。结果与对照组相比,db/db组LXRα蛋白表达量、ABCA1 mRNA表达水平明显下调(P<0.05);与db/db组相比,db/db+T0901317组上述指标表达上调(P<0.05);与db/db组相比,T0901317组LXRβ蛋白表达差异无统计学意义(P>0.05),而对照组LXRβ蛋白下调(P<0.05)。结论 LXR可能通过激活LXRα进而上调ABCA1以减轻糖尿病引起的肾脏炎症性损害,为拮抗糖尿病所致的肾脏炎症性损伤提供新的理论依据。Objective To investigate the effects of liver X receptor(LXR)agonist T0901317 on the expressions and activities of liver Xreceptor(LXR)in the kidney of db/db mice.Methods We divided the 8-week old male db/db mice into db/db group and db/db 2 T0901317 group(7 in each group).At the same time,we took 7 male wild-type C57BL/6 as control db/db group and the control group were administrated with 50(1 saline/animal by lavage for 7 days T0901317 group were given 12.5 mg T0901317/kg/day by lavage for7 days.After4 weeks,the expression levels of ABCA1 mRNA and LXR(and LXR(proteins in the kidney tissues were examined by using RT-PCRand Western blot analysis,respectively.Results Compared witli the control group,the mRNA expression of ABCA1 and the expression of LXRct were significantly decreased in the db/db group(P<0.05).However,compared with the db/db group,the mRNAlevel of ABCA1 and the production of LXRct were significantly increased in the db/db+T0901317 group(P<0.05).Compared with the db/db group,the expression of LXR#in the db/db 2 T0901317 group was unchanged(P>0.05)while in control group was decreased(P<0.LXRct to increase the expression of ABCA1 that reduces the inflammatory injury in diabetic nephropathy.The results may provide a novel theoretical basis for anti-inflammatory target therapy of diabetic nephropathy.
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