Chrysin, an anti-inflammatory molecule, abrogates renal
dysfunction in type 2 diabetic rats
Volume 279, Issue 1, 15 August 2014, Pages 1–7
Diabetic nepropathy (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, the 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 16 weeks 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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