Fenofibrate attenuates diabetic nephropathy in experimental diabetic rat's model via suppression of augmented TGF-β1/Smad3 signaling pathway

References

• Adler S. (1994). Structure-function-relationships associated with extracellular-matrix alterations in diabetic glomerulopathy. J Am Soc Nephrol, 5:1165–72
   PubMed Web of Science ®Google Scholar
• American Diabetes Association (ADA). (2003). Diabetic nephropathy. Diabetes Care, 26:S94–8
   Google Scholar
• Athyros VG, Tziomalos K, Karagiannis A, Mikhailidis DP. (2011). Dyslipidemia of obesity metabolic syndrome and type 2 diabetes mellitus: The case for residual risk reduction after statin treatment. Open Cardiovasc Med J, 5:24–34
   PubMedGoogle Scholar
• Attisano L, Wrana JL. (2002). Signal transduction by the TGF-beta superfamily. Science, 296:1646–7
   PubMed Web of Science ®Google Scholar
• Balakumar P, Chakkarwar VA, Singh M. (2009). Ameliorative effect of combination of benfotiamine and fenofibrate in diabetes-induced vascular endothelial dysfunction and nephropathy in the rat. Mol Cell Biochem, 320:149–62
   PubMed Web of Science ®Google Scholar
• Bartels H, Bohmer M. (1972). Serum creatinine determination without protein precipitation. Clin Chem Acta, 37:193–7
   PubMed Web of Science ®Google Scholar
• Carling DE, Rothrock CS, MacNish GC, et al. (1994). Characterisation of anastomosis group 11 (AG-11) of Rhizoctonia solani. Phytopathology, 84:1387–93
   Web of Science ®Google Scholar
• Chen HY, Huang XR, Wang W, et al. (2011). The protective role of Smad7 in diabetic kidney disease: Mechanism and therapeutic potential. Diabetes, 60:590–601
   PubMed Web of Science ®Google Scholar
• Chen LL, Zhang JY, Wang BP. (2006). Renoprotective effects of fenofibrate in diabetic rats are achieved by suppressing kidney plasminogen activator inhibitor-1. Vasc Pharmacol, 44:309–15
   PubMed Web of Science ®Google Scholar
• Chen YJ, Quilley J. (2008). Fenofibrate treatment of diabetic rats reduces nitrosative stress, renal cyclooxygenase expression and enhanced renal prostaglandin release. J Pharmacol Exp Therap, 324:658–63
   PubMed Web of Science ®Google Scholar
• Doumas BT, Watson WA, Biggs HG. (1971). Albumin standards and the measurement of serum albumin with bromcresol green. Clin Chim Acta, 31:87–96
   PubMed Web of Science ®Google Scholar
• Fazio S, Linton MF. (2010). High-density lipoprotein therapeutics and cardiovascular prevention. J Clin Lipidol, 4:411–9
   PubMed Web of Science ®Google Scholar
• Foster LB, Hochholzer JM. (1971). A single-reagent manual method for directly determining urea nitrogen in serum. Clin Chem, 17:921–5
   PubMed Web of Science ®Google Scholar
• Galkina E, Ley K. (2006). Leukocyte recruitment and vascular injury in diabetic nephropathy. J Am Soc Nephrol, 17:368–77
   PubMed Web of Science ®Google Scholar
• Gilliland G, Perrin S, Blanchard K, Bunn HF. (1990). Analysis of cytokine mRNA and DNA: Detection and quantitation by competitive polymerase chain reaction. Proc Natl Acad Sci USA, 87:2725–9
   PubMed Web of Science ®Google Scholar
• Goldfarb S, Ziyadeh FN. (2001). TGF-beta: A crucial component of the pathogenesis of diabetic nephropathy. Trans Am Clin Climatol Assoc, 112:27–32
   PubMedGoogle Scholar
• Guan Y, Breyer MD. (2001). Peroxisome proliferator-activated receptors (PPARs): Novel therapeutic targets in renal disease. Kidney Int, 60:14–30
   PubMed Web of Science ®Google Scholar
• Hakim ZS, Patel BK, Goyal RK. (1997). Effects of chronic ramipril treatment in streptozotocin-induced diabetic rats. Indian J Physiol Pharmacol, 41:353–60
   PubMedGoogle Scholar
• Hao HH, Shao ZM, Tang DQ, et al. (2012). Preventive effects of rutin on the development of experimental diabetic nephropathy in rats. Life Sci, 91:959–67
   PubMed Web of Science ®Google Scholar
• Hocher B, Thöne-Reineke C, Rohmeiss P, et al. (1997). Endothelin-1 transgenic mice develop glomerulosclerosis, interstitial fibrosis, and renal cysts but not hypertension. J Clin Invest, 99:1380–9
   PubMed Web of Science ®Google Scholar
• Isono M, Chen S, Hong SW, et al. (2002). Smad pathway is activated in the diabetic mouse kidney and Smad3 mediates TGF-beta-induced fibronectin in mesangial cells. Biochem Biophys Res Commun, 296:1356–65
   PubMed Web of Science ®Google Scholar
• Kadian S, Mahadevan N, Balakumar P. (2013). Differential effects of low dose fenofibrate treatment in diabetic rats with early onset nephropathy and established nephropathy. Eur J Pharmacol, 698:388–96
   PubMed Web of Science ®Google Scholar
• Kastarinen H, Ukkola O, Kesäniemi YA. (2009). Glomerular filtration rate is related to carotid intima-media thickness in middle-aged adults. Nephrol Dial Transplant, 24:2767–72
   PubMed Web of Science ®Google Scholar
• Kouroumichakis I, Papanas N, Zarogoulidis P, et al. (2012). Fibrates: Therapeutic potential for diabetic nephropathy? Eur J Int Med, 23:309–16
   PubMed Web of Science ®Google Scholar
• Lehir M, Kriz W. (2007). New insights into structural patterns encountered in glomerulosclerosis. Curr Opin Nephrol Hypertens, 16:184–91
   PubMed Web of Science ®Google Scholar
• Li L, Emmett N, Mann D, Zhao X. (2009). Fenofibrate attenuates tubulointerstitial fibrosis and inflammation through suppression of nuclear factor-κB and transforming growth factor-β1/Smad3 in diabetic nephropathy. Exp Biol Med (Maywood), 235:383–91
   Web of Science ®Google Scholar
• Long AN, Dagogo-Jack S. (2011). Comorbidities of diabetes and hypertension: Mechanisms and approach to target organ protection. J Clin Hypertens (Greenwich), 13:44–251
   Web of Science ®Google Scholar
• Manoj J. (2012). Histopathological changes in diabetic kidney disease. Clin Queries Nephrol, 0102:127–33
   Google Scholar
• Mauer SM. (1994). Structural-functional correlations of diabetic nephropathy. Kidney Int, 45:612–22
   PubMed Web of Science ®Google Scholar
• Milionis HJ, Elisaf MS. (2000). Management of hypertension and dyslipidaemia in patients presenting with hyperuricemia: Case histories. Curr Med Res Opin, 16:164–70
   PubMed Web of Science ®Google Scholar
• Mora C, Navarro J F. (2005). The role of inflammation as a pathogenic factor in the development of renal disease in diabetes. Curr Diab Rep, 5:399–401
   PubMedGoogle Scholar
• Moustakas A, Heldin CH. (2008). Dynamic control of TGF-beta signaling and its links to the cytoskeleton. FEBS Lett, 582:2051–65
   PubMed Web of Science ®Google Scholar
• Park CW, Kim HW, Ko SH, et al. (2006a). Accelerated diabetic nephropathy in mice lacking the peroxisome proliferator activated receptor alpha. Diabetes, 55:885–93
   PubMed Web of Science ®Google Scholar
• Park CW, Kim HW, Ko SH, et al. (2006b). Accelerated diabetic nephropathy in mice lacking the peroxisome proliferator-activated receptor alpha. Diabetes, 55:885–93
   PubMed Web of Science ®Google Scholar
• Park CW, Zhang Y, Zhang X, et al. (2006c). PPARalpha agonist fenofibrate improves diabetic nephropathy in db/db mice. Kidney Int, 69:1511–7
   PubMed Web of Science ®Google Scholar
• Paueksakon P, Revelo MP, Ma LJ, et al. (2002). Microangiopathic injury and augmented PAI-1 in human diabetic nephropathy. Kidney Int, 61:2142–8
   PubMed Web of Science ®Google Scholar
• Sharma K, Mc Gowan TA. (2000). TGF-beta in diabetic kidney disease: Role of novel signaling pathways. Cytokine Growth Factor Rev, 11:115–23
   PubMed Web of Science ®Google Scholar
• Sharma K, Ziyadeh FN. (1995). Hyperglycemia and diabetic kidney disease. The case for transforming growth factor-beta as a key mediator. Diabetes, 44:1139–46
   PubMed Web of Science ®Google Scholar
• Sowers JR, Epstein M. (1995). Diabetes mellitus and associated hypertension, vascular disease, and nephropathy. An update. Hypertension, 26:869–79
   PubMed Web of Science ®Google Scholar
• Tenenbaum A, Fisman EZ. (2004). Which is the best lipid-modifying strategy in metabolic syndrome and diabetes: Fibrates, statins or both? Cardiovasc Diabetol, 3:10. doi:10.1186/1475-2840-3-10
   PubMed Web of Science ®Google Scholar
• Tietz NM. (1990). Clinical guide to laboratory test. 2nd edn. Philadelphia, PA: WB Saunders Co., 246–50
   Google Scholar
• Wild S, Roglic G, Green A, et al. (2004). Global prevalence of diabetes: Estimates for the year 2000 and projections for 2030. Diabetes Care, 27:1047–53
   PubMed Web of Science ®Google Scholar
• Yang F, Chung AC, Ru Huang X, Lan HY. (2009). Angiotensin II induces connective tissue growth factor and collagen I expression via transforming growth factor-{beta}-dependent and –independent Smad pathways. The role of Smad3. Hypertension, 54:877–84
   PubMed Web of Science ®Google Scholar
• Zelmanovitz T, Gerchman F, Balthazar AP, et al. (2009). Diabetic nephropathy. Diabetol Metab Syndr, 1:10. doi:10.1186/1758-5996-1-10
   PubMed Web of Science ®Google Scholar
• Zhao X, Li LY. (2008). PPAR-alpha agonist fenofibrate induces renal CYP enzymes and reduces blood pressure and glomerular hypertrophy in Zucker diabetic fatty rats. Am J Nephrol, 28:598–606
   PubMed Web of Science ®Google Scholar
• Ziyadeh F, Han DC. (1997). Involvement of transforming growth factor-b and its re- 847 ceptors in the pathogenesis of diabetic nephropathy. Kidney Int, 52:848
   Google Scholar