1. Psidial A shows activity to enzyme PTP1B.
2. Psidial A reduces tumor growth and stimulate uterus proliferation.
1. Calycosin acts as a selective estrogen receptor modulator.
2. Calycosin induces apoptosis in human ovarian cancer SKOV3 cells by activating caspases and Bcl-2 family proteins.
3. Calycosin suppresses breast cancer cell growth via ERβ-dependent regulation of IGF-1R, p38 MAPK and PI3K/Akt pathways.
4. Calycosin has antineoplastic effects against osteosarcoma through inducing apoptosis showing in vitro and in vivo investigations.
5. Calycosin was shown to induce angiogenesis in human umbilical vein endothelial cell cultures (HUVEC) in vitro.
6. Calycosin may be an effective skin-lightening agent that regulates the expression of melanogenic enzymes. Calycosin exhibited tyrosinase inhibitory activity with an IC(50) value of 38.4 microM.
7. Calycosin has neuroprotective effects in cerebral ischemia/reperfusion rats, and the molecular mechanisms may correlate with the positive feedback between ER-α and miR-375, along with the regulation of downstream targets.
8. Calycosin is a vasorelaxant, it is also a noncompetitive Ca(2+) channel blocker.
1. Liquiritigenin can dose dependently alleviate mechanical, thermal and cold hyperalgesia, it may be potentially useful novel treatments for neuropathic pain.
2. Liquiritigenin possesses anti-inflammatory, antihyperlipidemic, and antiallergic effects.
3. Liquiritigenin decreases TNBS-induced phosphorylation of IKKβ, p65, and IκB-α.
4. Liquiritigenin is an estrogenic compound which acts as an agonist selective for the β-subtype of the estrogen receptor.
5. Liquiritigenin exhibits antitumour action in pituitary adenoma cells via Ras/ERKs and ROS-dependent mitochondrial signalling pathways.
6. Liquiritigenin possesses cytotoxic activity against five human cancer cell lines in vitro, inhibits the cell growth of SGC-7901 and Lovo.
1. Trans-Hinokiresinol is leukotriene B4 binding inhibitor and anti-fungal agent.
2. Trans-Hinokiresinol is an estrogen agonist，by stimulating the proliferation of estrogen-dependent T47D breast cancer cells, and their stimulatory effects were blocked by an estrogen antagonist.
1. Medicarpin biosynthesis has been induced in the shoots and reduced in the roots of the plants treated with a toxic concentration of Pb.
2. Medicarpin sensitizes myeloid leukemia cells to TRAIL-induced apoptosis through the upregulation of DR5 through activation of the ROS-JNK-CHOP pathway.
3. Medicarpin stimulates osteoblast differentiation likely via ERβ, promotes achievement of peak bone mass, and is devoid of uterine estrogenicity. In addition, given its excellent oral bioavailability, Medicarpin can be potential osteogenic agent.