Fisetin quarterhydrate inhibits lipid accumulation and suppresses the expression of PPARγ in 3T3-L1 cells. Fisetin quarterhydrate suppresses early stages of preadipocyte differentiation, and induces expression of Sirt1. Fisetin quarterhydrate facilitates Sirt1-mediated deacetylation of PPARγ and FoxO1, and enhances the association of Sirt1 with the PPARγ promoter, leading to suppression of PPARγ transcriptional activity, thereby repressing adipogenesis[1]. Fisetin quarterhydrate binds to tubulin and stabilizes microtubules with binding characteristics far superior than paclitaxel. Fisetin quarterhydrate treatment of human prostate cancer cells results in robust up-regulation of microtubule associated proteins (MAP)-2 and -4. Fisetin quarterhydrate significantly inhibits PCa cell proliferation, migration, and invasion. Nudc, a protein associated with microtubule motor dynein/dynactin complex that regulates microtubule dynamics, is inhibited with Fisetin quarterhydrate treatment[2].
Fisetin quarterhydrate treatment to UVB exposed mice results in decreased hyperplasia and reduces infiltration of inflammatory cells. Fisetin quarterhydrate treatment also reduces inflammatory mediators such as COX-2, PGE2 as well as its receptors (EP1- EP4), and MPO activity. Furthermore, Fisetin quarterhydrate reduces the level of inflammatory cytokines TNFα, IL-1β and IL-6 in UVB exposed skin. Fisetin quarterhydrate treatment also reduces cell proliferation markers as well as DNA damage as evidenced by increased expression of p53 and p21 proteins[3].
References:
[1]. Kim SC, et al. Fisetin induces Sirt1 expression while inhibiting early adipogenesis in 3T3-L1 cells. Biochem Biophys Res Commun. 2015 Nov 27;467(4):638-44.
[2]. Mukhtar E, et al. Dietary flavonoid fisetin binds to β-tubulin and disrupts microtubule dynamics in prostate cancer cells. Cancer Lett. 2015 Oct 28;367(2):173-83.