Coompo Research Chemicals

Syringaresinol inhibits Helicobacter pylori motility.
Syringaresinol induces vasorelaxation by enhancing NO production in endothelial cells via two distinct mechanisms, phosphatidylinositol 3-kinase/Akt- and PLC/Ca(2+)/CaMKKβ -dependent eNOS phosphorylation and Ca(2+)-dependent eNOS dimerization.
Syringaresinol showed inhibitory effects on the P-glycoprotein in adriamycin-resistant human breast cancer cells, MCF-7/ADR.

(-)-Syringaresinol decreased the viability of HL-60 cells by inducing G1 arrest followed by apoptosis in a dose- and time-dependent manner. The G0/G1 phase of the cell cycle is regulated by cyclin-dependent kinases (Cdk), cyclins and cyclin-dependent kinase inhibitors (Cdki). We show by western blot analysis, that the (-)-syringaresinol-induced G1 arrest was mediated through the increased expression of Cdki proteins (p21cip1/waf1 and p27kip1) with a simultaneous decrease in cdk2, cdk4, cdk6, cyclin D1, cyclin D2, and cyclin E expression. The induction of apoptosis after treatment with (-)-syringaresinol for 24 h was demonstrated by morphological changes, DNA fragmentation, altered ratio of Bax/Bcl-2, cleavage of poly(ADP-ribose) polymerase and flow cytometry analysis. (-)-Syringaresinol also induced cytochrome c release and activation of caspase-3 and caspase-9. To our knowledge, this is the first time that (-)-syringaresinol has been reported to potently inhibit the proliferation of human promyelocytic HL-60 cells through G1 arrest and induction of apoptosis. These findings suggest that (-)-syringaresinol may be a potential chemotherapeutic agent for the treatment of cancer.