Research of revolutionary kidney regeneration for hereditary nephritis using a mouse model

近年来的研究发现核因子κB（NF-κB）的活化在微小病变型肾病综合征（MCNS）中起重要作用，有理论认为激素治疗MCNS的疗效与抑制NF-κB活性有关。去羟甲基环氧喹诺霉素（DHMEQ）是一种新开发的NF-κB抑制剂，可直接与NF-κB组分特异性结合而抑制DNA结合。因此，它被认为是比大多数其他NF-κB抑制剂更具体。我们进行了这项研究，以确定DHMEQ是否可以改善嘌呤霉素氨基糖苷（PAN）诱导的肾病小鼠模型MCNS。结果表明，DHMEQ能明显减少小鼠的蛋白尿，改善高胆固醇血症和低蛋白血症。DHMEQ还抑制PAN诱导的NF-κB从细胞质向细胞核的移位。结论：NF-κB在MCNS的发病机制中起重要作用，DHMEQ是治疗MCNS的有效药物。

Recent observations have revealed that the activation of nuclear factor κB (NF-κB) plays an important role in minimal- change nephrotic syndrome (MCNS), and there is a theory that therapeutic efficacy of steroids in MCNS is associated with the inhibition of NF-κB activity. Dehydroxy-methyl-epoxyquinomicin (DHMEQ) is a newly developed inhibitor of NF-κB that directly binds specifically to NF-κB components to inhibit DNA binding. Therefore, it is thought to be more specific than most other NF-κB inhibitors.We conducted this study to determine whether DHMEQ may ameliorate puromycin aminonucleoside (PAN)-induced nephrosis in a murine model for MCNS. As a result, DHMEQ could reduce the albuminuria and ameliorate the hypercholesterolemia and hypoalbuminemia in comparison with PAN injection without DHMEQ in the mice. DHMEQ also inhibited PAN-induced NF-κB translocation from the cytoplasm to the nucleus. In conclusion, NF-κB plays an important role in the pathogenesis of MCNS, and these results suggest that DHMEQ is a candidate therapeutic agent for MCNS.