Conclusion: Fisetinlowereduricemia, suppressed renal inflammatory response, and improvedkidney fibrosis to protect against hyperuricemic nephropathy via modulation of STAT3 and TGF-β signalingpathways. The results highlighted that fisetin might represent a potential therapeutic strategy against hyperuricemic nephropathy.»
«Firstly, we evaluated the effect of fisetin on IL-1β-induced NO, PGE2, IL-6, TNF-α production in human OA chondrocytes. Chondrocytes were pretreated with various concentration of fisetin (1, 5, 10 μM) for 2 h, followed by stimulation with or without IL-1β (10 ng/ml) for 24 h.
The NO concentration in the surpernatant was detected using the Griess Reagent and the production of PGE2, IL-6, TNF-α in the medium was measured by ELISAs. As shown in Fig. 2A–D, the production of NO, PGE2, IL-6, TNF-α elevatedsignificantly compared with the control group after IL-1β treatment. However, fisetindose-dependently inhibitedIL-1β-induced NO, PGE2, IL-6, TNF-α levels in the medium..»