Quercetin

Quercetin significantly down regulates myofibroblast differentiation and fibrotic markers, such as alpha-smooth muscle actin (alpha-SMA) and Collagen III (Col III), in both HCFs and HKCs. Collagen III secretion was reduced 80% in both HCFs and HKCs following Quercetin treatment.Furthermore, Quercetin reduced lactate production by HKCs to normal HCF levels. Quercetin down regulated TGF-betaR2 and TGF-beta2 expression in HKCs suggesting a significant link to the TGF-beta pathway. Quercetin is a key regulator of fibrotic markers and ECM assembly by modulating cellular metabolism and TGF-beta signaling. Quercetin strongly abrogated PI3K and Src kinases, mildly inhibited Akt1/2, and slightly affected PKC, p38 and ERK1/2. Quercetin or the combined use of adenosine diphosphate and thromboxane A(2) inhibitors abrogated platelet spreading on these surfaces to a similar extent. The inhibitory effect of quercetin on platelet kinases blocks early signaling events preventing a complete platelet spreading. PKC inhibitors H-7 and quercetin protect BPAEC from TNF induced injuries and PKC play an important role in EC activation by TNF.

Meletin, Sophoretin

C15H10O7

>98%