作者: Koji Hashimoto , Yuji Kamijo , Takero Nakajima , Makoto Harada , Makoto Higuchi
DOI: 10.1155/2012/976089
关键词: Nephritis 、 IκBα 、 Clofibrate 、 Mesangial proliferative glomerulonephritis 、 Receptor 、 Signal transduction 、 Endocrinology 、 Internal medicine 、 Kidney disease 、 Medicine 、 Glomerulonephritis
摘要: The vast increase of chronic kidney disease (CKD) has attracted considerable attention worldwide, and the development a novel therapeutic option against representative that leads to CKD, mesangial proliferative glomerulonephritis (MsPGN) would be significant. Peroxisome proliferator-activated receptor α (PPARα), member steroid/nuclear superfamily, is known perform various physiological functions. Recently, we reported PPARα in activated cells exerted anti-inflammatory effects deficiency resulted high susceptibility glomerulonephritis. To investigate whether activation improves activity MsPGN, examined protective agonist, clofibrate, well-established model human anti-Thy1 nephritis, for first time. This study demonstrated pretreatment with clofibrate (via 0.02% or 0.1% clofibrate-containing diet) continuously glomerular PPARα, which outweighed deterioration associated nephritic process. appeared suppress NF-κB signaling pathway glomeruli by induction IκBα, resulting reduction proteinuria amelioration active inflammatory pathologic changes. These findings suggest antinephritic potential PPARα-related medicines MsPGN. might useful as treatment CKD.