Abstract
The present study was to investigate the protection of resveratrol (RSV) in diabetes associated with kidney inflammation and cell proliferation. Rat mesangial cell and streptozotocin-induced type 1 diabetes mouse model were used. In vitro, RSV attenuated high glucose-induced plasminogen activator inhibitor (PAI-1) expression and mesangial cell proliferation, as well as Akt and nuclear factor-kappa B (NF-κB) activation. The similar results were recaptured in the experiment with Akt inhibitors. In vivo, mice were divided into three groups: control group, diabetes mellitus (DM) group, and RSV-treated DM group. Compared with control group, the kidney weight to body weight ratio and albumin to creatinine ratio were increased in DM group, but not in RSV-treated DM group. Furthermore, the increased expression of PAI-1 and intercellular adhesion molecule-1 in diabetic renal cortex were also reduced by RSV administration. Besides, the kidney p-Akt/Akt ratio and NF-κB were significantly increased in DM group; however, these changes were reversed in RSV-treated DM group. Additionally, immunohistochemistry results indicated that RSV treatment reduced the density of proliferating cell nuclear antigen-positive cells significantly in glomeruli of diabetic mice. These results suggest that RSV prevents diabetes-induced renal inflammation and mesangial cell proliferation possibly through Akt/NF-κB pathway inhibition.
Highlights
Nowadays, diabetic nephropathy (DN) has become a serious problem worldwide because of its rapidly increasing rates, as well as economic and social burden
We provided evidence here that exposure to HG significantly increased the expression of NF-κB and its downstream gene PAI-1
We reported that the Akt activity inhibitors could inhibit HG-induced renal mesangial cell proliferation and NF-κB activity
Summary
Diabetic nephropathy (DN) has become a serious problem worldwide because of its rapidly increasing rates, as well as economic and social burden. The intimate mechanisms leading to the development and progression of this disease are complex and not yet fully understood [1]. Glomerular mesangium expansion is one of the characters of early DN. Accumulated data suggest that the predicted evolution of diabetic glomerulopathy is comprised of an early, transient mesangial cell proliferation and subsequent hypertrophy of these cells that herald the slow progression into glomerulosclerosis [2]. Inflammation is an important pathophysiological factor in the development and progression of DN [3, 4]. Recent studies have emphasized the critical roles of inflammatory response in development of DN [5, 6]. Different inflammatory molecules, including chemokines, adhesion molecules, and proinflammatory cytokines, may be critical factors involved in DN
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