Trifolirhizin, a pterocarpan flavonoid, was isolated from the roots of Sophora flavescens. Trifolirhizin not only dose-dependently inhibited LPS-induced expression of pro-inflammatory cytokines including tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) but also inhibited lipopolysaccharide (LPS)-induced expression of cyclooxygenase-2 (COX-2). In addition, trifolirhizin showed in vitro inhibitory effects on the growth of human A2780 ovarian and H23 lung cancer cells[2]. Trifolirhizin caused a significantly decreased proliferation of MKN45 cells in a time- and dose-dependent manner, with IC50 values of 33.27±2.06 µg/mL at 48 h[3]. Moreover, trifolirhizin is an active constituent that inhibits acetylcholine mediated ASM (airway smooth muscle) contraction or directly relaxes pre-contracted ASM independent of β2-adrenoceptors[4].
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