慢性肾炎是常见的多发病，疑难病，不及时治疗最终将发展为慢性肾衰竭。故防止和延缓肾功能衰竭的发生，开发能有效防治肾病的药物迫在眉睫。蒙医药学在肾脏疾病的诊治方面有其独特认识，治疗肾病的有效复方制剂也较多。本课题组在前期研究工作中发现蒙药制剂那仁满都拉对急慢性肾功能损伤有保护作用，但其作用机制尚不明了。本课题研究中，拟通过注射C-BSA建立慢性肾炎大鼠模型，从尿液指标、血液指标、组织病理学及相关蛋白质表达水平等方面观察那仁满都拉对实验性慢性肾炎的治疗作用。进而应用miRNA微阵列芯片技术，筛选各实验组大鼠差异表达的miRNAs，在差异表达谱中寻找出在系膜细胞中高表达的靶基因，以探索该蒙药对系膜细胞的增殖、凋亡的影响及对IL-10介导的NF-kB信号通路的作用，从而揭示蒙药那仁满都拉对慢性肾炎大鼠免疫炎症的防治作用机制。为其临床应用及进一步研发提供科学依据。

Chronic nephritis is a common frequently-occurring disease, venereology, not treated will eventually develop into chronic kidney failure. Therefore, to prevent and delay the onset of renal failure, and develop the drugs its can effectively prevent and treat the kidney disease is imminent. Mongolian medicine has its unique understanding in the diagnosis and treatment of kidney disease, its also have variety of effective compound preparation to treat the kidney disease. Our researchers found Narenmandula have a protective effect from acute or chronic renal injury. But its mechanism is still unknown. This topic research, proposed by injecting a C-BSA to establish the rat model with chronic nephritis, from urine, blood, tissue pathology and related protein expression levels and observed that Mongolian medicine Narenmandula’s therapeutic effect on treating chronic nephritis. Screening and application of miRNA microarray chip technology, the experimental group rats differentially expressed miRNAs, finds out differences in expression in mesangial cells high expression of target genes, to explore the Mongolian affect mesangial cell proliferation, apoptosis and NF-kB of IL-10 mediated signaling pathway, so as to reveal the Mongolian medicine Narenmandula that benevolence, full of immune inflammation in the prevention and control of chronic nephritis rats and the effect mechanism. To provide a scientific basis for its clinical application and further development.

慢性肾炎是极为常见的多发病,疑难病，不及时治疗最终将发展为慢性肾衰竭，也是终末期慢性肾衰竭的主要病因开发能有效防治肾病的药物迫在眉睫。本研究建立C-BSA所致慢性肾炎大鼠模型，采用生化分析法，酶联免疫法，免疫组化法，RT-PCR 法等研究方法，研究其大鼠尿液、血液、组织的相关指标，初步阐明蒙药那仁满都拉对C-BSA所致慢性肾炎大鼠肾功能保护作用及作用机制。结果该药物有不同程度的增加慢性肾炎模型大鼠体重，降低24ｈ尿蛋白含量；增加血清BAL含量，降低血清BUN、Gre含量和尿液PRO、BIL的含量；通过増加抗炎因子IL-10合成分泌，减少促炎因子IL-2、IL-6、TNF-α，抑制C-BSA所致慢性肾炎大鼠的免疫炎症反应，继而减轻肾脏免疫损伤；减低尿液β2-MG、补体C3含量，抑制肾小球系膜细胞增生、系膜基质增多，肾小管上皮细胞空化及炎细胞浸润；通过下调肾脏组织NF-kB、TGF-β1和IL-2mRAN的表达，上调MMP-9和IL-10 mRAN的表达，改善肾脏组织病理病变；认为该药物的治疗慢性肾炎的作用机制与NF-kB、TGF-β1、MMP-9和IL-2mRAN、IL-10 mRAN的表达有关，从而对C-BSA所致慢性肾炎有肾脏保护作用。本研究为该药物的临床应用及进一步开发研究提供了可靠而丰富的实验依据。