论文部分内容阅读
目的观察炎症因子白细胞介素-1β(interleukin-1 beta,IL-1β)在阿霉素肾病大鼠发生肾小球硬化过程中的表达,探讨辛伐他汀保护阿霉素肾病大鼠肾脏的机制。方法雄性SD大鼠分为正常对照组、阿霉素肾病组(模型组)和阿霉素肾病辛伐他汀治疗组(治疗组),分别灌胃给药11周。免疫组化法观测肾组织中IL-1β的定位表达,半定量RT-PCR技术检测肾组织IL-1β mRNA的表达,酶联免疫吸附法检测血清和肾组织中IL-1β的水平,光镜观察肾小球硬化的情况。结果模型组肾组织IL-1β的表达明显增强(P<0.01),伴有明显的肾小球硬化及肾功能损害(P<0.01);与模型组比较,治疗组肾组织IL-1β的表达、肾小球硬化及肾功能损害均减轻(分别P<0.05、P<0.01、P<0.05)。结论辛伐他汀可能通过降低肾组织内IL-1β的表达,对肾脏起保护作用。
Objective To observe the expression of interleukin-1β (IL-1β) in adriamycin-induced nephropathy rats during glomerulosclerosis and explore the mechanism of simvastatin in protecting adriamycin-induced nephropathy rat kidney . Methods Male Sprague-Dawley rats were divided into normal control group, adriamycin nephropathy group (model group) and simvastatin treatment group (treatment group). The rats were administered intragastrically for 11 weeks. The expression of IL-1β in renal tissue was detected by immunohistochemistry. The expression of IL-1β mRNA in renal tissue was detected by semi-quantitative RT-PCR. The levels of IL-1β in serum and kidney were detected by enzyme-linked immunosorbent assay. Observe the situation of glomerulosclerosis. Results The expression of IL-1β in renal tissue of model group was significantly increased (P <0.01), with obvious glomerulosclerosis and renal dysfunction (P <0.01). Compared with model group, the expression of IL-1β , Glomerular sclerosis and renal dysfunction were reduced (P <0.05, P <0.01, P <0.05, respectively). Conclusion Simvastatin may protect the kidneys by reducing the expression of IL-1β in renal tissues.