Chrysin, an anti-inflammatory molecule, abrogates renal
dysfunction in type 2 diabetic rats
Toxicol Appl Pharmacol, 2014 May 18. pii:
S0041-008X(14)00191-4
Diabetic nephropathy (DN) is considered as the leading cause
of end-stage renal disease (ESRD) worldwide, but the current available
treatments are limited. Recent experimental evidences support the role of
chronic microinflammation in the development of DN. Therefore, tumor necrosis
factor-alpha (TNF-α) pathway has emerged as a new therapeutic target for the
treatment of DN.
We investigated the nephroprotective effects of chrysin (5,
7-dihydroxyflavone) in a high fat diet/streptozotocin (HFD/STZ)-induced type 2
diabetic Wistar albino rat model. Chrysin is a potent anti-inflammatory
compound that is abundantly found in plant extracts, honey and bee propolis.
The treatment with chrysin for 16weeks post induction of diabetes significantly
abrogated renal dysfunction and oxidative stress. Chrysin treatment
considerably reduced renal TNF-α expression and inhibited the nuclear
transcription factor-kappa B (NF-кB) activation. Furthermore, chrysin treatment
improved renal pathology and suppressed transforming growth factor-beta
(TGF-β), fibronectin and collagen-IV protein expressions in renal tissues.
Chrysin also significantly reduced the serum levels of pro-inflammatory
cytokines, interleukin-1beta (IL-1β) and IL-6. Moreover, there were no
appreciable differences in fasting blood glucose and serum insulin levels
between the chrysin treated groups compared to the HFD/STZ-treated group.
Hence, our results suggest that chrysin prevents the development of DN in
HFD/STZ-induced type 2 diabetic rats through anti-inflammatory effects in the
kidney by specifically targeting the TNF-α pathway.
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