title: Improvement of inflammatory responses associated with NF-kappa B pathway in kidneys from diabetic rats.
abstract: OBJECTIVE
  The effects of fenofibrate on the kidneys of diabetic rats were investigated by measuring the inflammatory responses associated with transcription factor nuclear factor kappa-B (NF-kappa B) pathway.
  
  
  METHODS
  Male Wistar rats were randomly divided into 3 groups: normal control, diabetes control and diabetes + fenofibrate (10 in each group). The expression of NF-kappaB p65, plasminogen activator inhibitor-1 (PAI-1), and intercellular adhesion molecule-1 (ICAM-1) in renal cortex was detected by Western blot, RT-PCR, and immunohistochemistry, respectively. Blood lipid profiles, glucose, and urine albumin were measured as well.
  
  
  RESULTS
  The expression of NF-kappa B p65, PAI-1, and ICAM-1 was significantly higher in the diabetes control than those in the normal control, and treatment with fenofibrate inhibited the increased expression of these factors in kidneys by 48.18 %, 35.04 %, and 26.41 %, respectively when compared with the diabetes control, although they were still higher in diabetes + fenofibrate than those in the normal control. Correspondingly, the profiles of lipid were significantly elevated in the diabetes control compared with the normal control, and decreased significantly in diabetes + fenofibrate.
  
  
  CONCLUSIONS
  Fenofibrate exhibited a downregulating effect on the NF-kappa B pathway in diabetic kidneys, implying that fenofibrate could be a potential treatment for diabetic nephropathy.
authors.affiliation: Department of Endocrinology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China. cheria_chen@126.com
authors.forename: L
authors.initials: L
authors.lastname: Chen
authors.forename: J
authors.initials: J
authors.lastname: Zhang
authors.forename: Y
authors.initials: Y
authors.lastname: Zhang
authors.forename: Y
authors.initials: Y
authors.lastname: Wang
authors.forename: B
authors.initials: B
authors.lastname: Wang
mesh_terms: D000818:Animals; D003921:Diabetes Mellitus, Experimental / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D003928:Diabetic Nephropathies / Q000188:drug therapy / Q000209:etiology; D004195:Disease Models, Animal; D011345:Fenofibrate / Q000494:pharmacology* / Q000627:therapeutic use; D000960:Hypolipidemic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D007249:Inflammation / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D007668:Kidney / Q000187:drug effects / Q000378:metabolism* / Q000503:physiopathology; D008297:Male; D016328:NF-kappa B / Q000378:metabolism*; D017395:Plasminogen Activator Inhibitor 1 / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D015398:Signal Transduction / Q000502:physiology; D013311:Streptozocin
chemical_list: D000960:Hypolipidemic Agents; D016328:NF-kappa B; D017395:Plasminogen Activator Inhibitor 1; D018799:Intercellular Adhesion Molecule-1; D013311:Streptozocin; D011345:Fenofibrate