<p style=/line-height:25px/>Quercetin is a flavonoid with anticancer activity; mitochondrial ATPase and phosphodiesterase inhibitor and Inhibits PI3-kinase activity and slightly inhibits PIP kinase activity.<br>IC50 value:<br>Target: anticancer natural compound<br>in vitro: Quercetin is a naturally derived PDE4-selective inhibitor found in fruits, vegetables, and tea. Addition of quercetin (100 nM-1 mM) acutely and concentration-dependently relaxed airway rings precontracted with ACh. In separate studies, pretreatment with quercetin (100 μM) prevented force generation upon exposure to ACh [1]. quercetin could induce apoptosis in A549 cells through mitochondrial depolarization by causing an imbalance in B-cell lymphoma 2/ Bcl2 Antagonist X (Bcl2/Bax) ratio and by down-regulating the interleukine-6/signal transducer and activator of transcription 3 (IL-6/STAT3) signaling pathway. quercetin could block nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) activity at early hours, which might cause a down-regulation of the IL-6 titer, and the IL-6 expression, in turn, could inhibit p-STAT3 expression [2]. quercetin significantly decreased the phosphorylation of ERK1/2 and FAK, a downstream ERK signaling protein. Inhibition of this pathway with U0126, an inhibitor of MAP kinase, retarded wound closure, whereas sustained p-ERK1/2 activation, induced by vanadate, restored astrocyte migration [4].<br>in vivo: quercetin directly attenuated phospholipase C activity, decreased inositol phosphate synthesis, and decreased intracellular calcium responses to Gq-coupled agonists (histamine or bradykinin). Finally, nebulization of quercetin (100 μM) in an in vivo model of airway responsiveness significantly attenuated methacholine-induced increases in airway resistance [1]. Rats, subjected to 24h of UUO, were treated i.p. with quercetin 50 mg/kg/day. Quercetin partly prevented COX-2 induction in renal inner medulla (IM) in response to UUO. Moreover, RMICs exposed to the conditions associated with obstruction, inflammation (produced by interleukin-1β (IL-1β)), oxidative-stress (produced by H2O2) and mechanical stress (produced by stretch) showed increased COX-2 expression [3].</p>
