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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