自噬在肾脏结石大鼠发病中的作用机制

发布时间：2018-11-08 13:41

【摘要】：目的探讨自噬在肾脏结石发病中的作用机制。方法建立腺嘌呤摄入过量引发的肾结石小鼠模型,通过对小鼠血液、尿液、肾脏组织样本收集,运用分子生物学方法检测小鼠血液中肌苷酸含量、小鼠体重、肾比重、一昼夜尿液量、小鼠尿液中微量蛋白含量及肾脏组织自噬基因mRNA和自噬相关蛋白的表达情况,并运用生物统计学进行数统计。结果腺嘌呤模型小鼠体重下降,肾比重和一昼夜排尿量比对照组较高,酶联免疫吸附(ELISA)结果显示腺嘌呤模型小鼠血液中肌苷酸的含量,尿液中微量蛋白的含量与对照组相比升高,同时PCR及蛋白免疫印迹结果证明自噬相关mRNA和蛋白表达量的变化,自噬抑制剂处理小鼠后,肾结石症状稍有缓解,自噬相关mRNA和蛋白表达量的也发生调整。结论证明2,8二羟基腺嘌呤结石的积累可以引起肾组织自噬发生,导致肾结石相关症状。
[Abstract]:Objective to investigate the mechanism of autophagy in the pathogenesis of renal calculi. Methods A mouse model of renal calculi induced by excessive adenine intake was established. The blood, urine and kidney tissue samples were collected, and the contents of inosine in blood, body weight and renal specific gravity of mice were detected by molecular biological method. The contents of microprotein in urine and the expression of autophagy gene mRNA and autophagy related protein in kidney tissue of mice were analyzed by biostatistics. Results the weight of adenine model mice was decreased, the renal specific gravity and urination volume in one day and night were higher than those in control group. The results of (ELISA) showed that the content of inosine in blood of adenine model mice was higher than that of control group. The content of trace protein in urine was higher than that in control group. PCR and Western blotting showed that the expression of autophagy related mRNA and protein was changed. The symptoms of renal calculi in mice treated with autophagy inhibitor were alleviated slightly. Autophagy related mRNA and protein expression were also regulated. Conclusion the accumulation of 2-dihydroxyadenine stone can induce autophagy in renal tissue and lead to renal calculi related symptoms.
【作者单位】：广东药科大学附属第一医院泌尿外科;
【基金】：广东省医学科学基金资助项目(No.B2012085)
【分类号】：R692.4

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