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Abstract
Advanced glycation end products (AGEs) play a causative role in the development of diabetic nephropathy via induction of matrix protein deposition in kidneys. This study investigated inhibitory effects of chrysin, present in bee propolis and herbs, on glomerulosclerosis in db/db mice and AGEs-exposed renal mesangial cells. The in vivo study explored the demoting effects of 10 mg/kg chrysin on glomerular fibrosis in a type 2 diabetic model. Oral supplementation of chrysin inhibited the collagen fiber accumulation and α-smooth muscle actin (α-SMA) induction in periodic acid schiff-positive renal tissues of db/db mice. Moreover, treating db/db mice with chrysin diminished the level of AGEs increased in diabetic glomeruli. The in vitro study employed human mesangial cells exposed to 100 μg/mL AGE-BSA for 72 h in the presence of 1–20 μM chrysin. Glucose increased mesangial AGE production via induction of receptor for AGEs. Chrysin suppressed the induction of collagens, α-SMA, fibroblast-specific protein-1 and matrix metalloproteinases enhanced by AGE-bovine serum albumin. Furthermore, chrysin blunted transforming growth factor-β1 induction and Smad 2/3 activation in AGEs-exposed mesangial cells. These results demonstrate that chrysin attenuated accumulation of myofibroblast-like cells and matrix proteins in AGEs-laden diabetic glomeruli. Therefore, chrysin may be a potential renoprotective agent targeting glucose-mediated AGEs-associated glomerulosclerosis and fibrosis.
Highlights
Diabetic nephropathy (DN), a serious diabetic complication and a progressive kidney disease, is characteristic of glomerulosclerosis and interstitial fibrosis [1,2]
This study investigated the suppressive effects of chrysin on glucose-promoted mesangial fibrosis
The current study examined that chrysin glucose-induced mesangial expansion and fibrosis through inhibiting Advanced glycation end products (AGEs) activation in kidneys
Summary
Diabetic nephropathy (DN), a serious diabetic complication and a progressive kidney disease, is characteristic of glomerulosclerosis and interstitial fibrosis [1,2]. The progressive renal dysfunction causes deposition of inflammatory cells within glomeruli, which develops proteinuria and glomerulosclerosis [3,4,5]. Hyperglycemia is the major factor responsible for structural alterations at the renal level and induces renal damage directly or through hemodynamic modifications such as increased glomerular filtration, shear stress and albuminuria [8,9]. These alterations contribute to an abnormal stimulation of resident renal cells including mesangial cells that produce more transforming growth factor (TGF)-β1 [10,11].
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