State Key Laboratory of Natural and Biomimetic Drugs, Department of Pharmacology, School of Basic Medical Sciences, Peking University, Beijing, 100191, China.
State Key Laboratory of Bioactive Substance and Function of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100050, China.
Kidney Int. 2017 Dec;92(6):1404-1418. doi: 10.1016/j.kint.2017.04.013. Epub 2017 Jul 12.
Autosomal dominant polycystic kidney disease (ADPKD) is a common monogenetic disease characterized by the progressive development of renal cysts with further need for effective therapy. Here our aim was to investigate the effect of Ganoderma triterpenes (GT) on the development of kidney cysts. Importantly, GT attenuated cyst development in two mouse models of ADPKD with phenotypes of severe cystic kidney disease. Assays for tubulogenesis showed that GT promoted epithelial tubule formation in MDCK cells, suggesting a possible effect on epithelial cell differentiation. The role of GT in regulating key signaling pathways involved in the pathogenesis of PKD was further investigated by immune blotting. This showed that GT specifically downregulated the activation of the Ras/MAPK signaling pathway both in vitro and in vivo without detectable effect on the mTOR pathway. This mechanism may be involved in GT downregulating intracellular cAMP levels. Screening of 15 monomers purified from GT for their effects on cyst development indicated that CBLZ-7 (ethyl ganoderate C2) had a potent inhibitory effect on cyst development in vitro. Additionally, like GT, CBLZ-7 was able to downregulate forskolin-induced activation of the Ras/MAPK pathway. Thus, GT and its purified monomer CBLZ-7 may be potential therapeutic regents for treating ADPKD.
常染色体显性多囊肾病(ADPKD)是一种常见的单基因疾病,其特征是肾囊肿的进行性发展,需要有效的治疗。在这里,我们的目的是研究灵芝三萜(GT)对肾囊肿发展的影响。重要的是,GT 减轻了两种 ADPKD 小鼠模型的肾囊肿发育,这些模型具有严重的囊性肾病表型。小管形成测定表明,GT 促进了 MDCK 细胞中上皮小管的形成,提示其可能对上皮细胞分化有影响。通过免疫印迹进一步研究了 GT 在调节 PKD 发病机制中涉及的关键信号通路的作用。结果表明,GT 特异性地下调了 Ras/MAPK 信号通路的激活,无论是在体外还是体内,对 mTOR 通路均无明显影响。该机制可能与 GT 下调细胞内 cAMP 水平有关。对从 GT 中纯化的 15 种单体进行筛选,以研究它们对囊肿发育的影响,结果表明 CBLZ-7(乙基灵芝 C2)对体外囊肿发育具有很强的抑制作用。此外,与 GT 一样,CBLZ-7 能够下调福司柯林诱导的 Ras/MAPK 通路的激活。因此,GT 和其纯化单体 CBLZ-7 可能是治疗 ADPKD 的潜在治疗试剂。