Improvement of inflammatory responses associated with NF-κB pathway in kidneys from diabetic rats

Abstract

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.

Immunoinflammation in Diabetic Nephropathy: Molecular Mechanisms and Therapeutic Options

“…Other studies demonstrated that 1,25-dihydroxyvitamin D3 suppresses hyperglycemia-induced gene expression by blocking NF-κB activation in mesangial cells (Zhang et al, 2007). Statins and fenofibrate also exhibit a downregulating effect on NF-κB pathway in kidneys from diabetic rats Chen et al, 2008). In the same way, a recent report demonstrates that the ameliorative effects of the plant alkaloid berberine on renal dysfunction in diabetic rats is associated with its inhibitory function on NF-κB signal pathway in the kidney (Liu et al, 2010).…”

Drugs for Diabetic Nephropathy- Full Review

“…[71] 3) Thiazolidinedione drugs Ameliorated renal injury in diabetic rats. [73] 4) Statin and fenofibrate down regulates NF-κB [72] 5) Plant alkaloid berberine inhibits NF-κB and ICAM-1 in diabetic rats and ameliorate renal dysfunction [65] From the above study and pathological role it is clear that up regulation of NF-κB in diabetic kidney and plays important role in development of diabetes nephropathy. Thus targeting NF-κB may retard development of nephropathy.…”

Antioxidant defenses in diabetes mellitus: a clinical and molecular approach

“…NFκB activation triggers potent inflammatory reactions found in acute pancreatitis, DM, metabolic syndrome, brain injury, Alzheimer's disease, and diabetic nephropathy [76]. Into the cortex of the kidneys, NFkB activation was associated with increased expression of plasminogen activator inhibitor-1 (PAI-1) and enhanced expression of the intercellular adhesion molecule-1 (ICAM-1) which were associated with higher degree of renal inflammation in diabetic rats [77]. The activation of p38-MAPK pathway also impairs insulin action into the myocardium increasing free radical-mediated infarction [78].…”