Licochalcone A from licorice root, an inhibitor of human hepatoma cell growth via induction of cell apoptosis and cell cycle arrest.

We investigated the anti-cancer activity of Licochalcone A (LCA), extracted from licorice root. LCA inhibited the proliferation of HepG2 cells with IC50 (65.96 µM) for 24 h and IC50 (44.13 µM) for 48 h and caused significant morphological changes and also led to intracellular ROS generation. LCA affected HepG2 cell growth by terminating cell cycle development at G2/M transition and further induced the apoptosis process. The mRNA expression of genes involved in cell cycles such as Survivin, Cyclin B1, and CDK1 were reduced; while, Weel, P21, Cyclin D1, and JNK1 showed increased mRNA expression. Two pathways consisting of internal and external factors were responsible for LCA -induced apoptosis. The anti-cancer action involved increased mRNA expression of DR3, DR5, caspases-3, caspases-8, caspases-10, Fas, Bad, Bax, Bcl-2, Bak, and PUMA; besides, decreased level of PKCε, p70S6K, and Akt. This study provides mechanistic explanation for anti-cancer activity of LCA and also suggests its potential role in the treatment of hepatoma cancer.

Early developmental bisphenol-A exposure sex-independently impairs spatial memory by remodeling hippocampal dendritic architecture and synaptic transmission in rats.

Bisphenol-A (BPA, 4, 4'-isopropylidene-2-diphenol), a synthetic xenoestrogen that widely used in the production of polycarbonate plastics, has been reported to impair hippocampal development and function. Our previous study has shown that BPA exposure impairs Sprague-Dawley (SD) male hippocampal dendritic spine outgrowth. In this study, the sex-effect of chronic BPA exposure on spatial memory in SD male and female rats and the related synaptic mechanism were further investigated. We found that chronic BPA exposure impaired spatial memory in both SD male and female rats, suggesting a dysfunction of hippocampus without gender-specific effect. Further investigation indicated that BPA exposure causes significant impairment of dendrite and spine structure, manifested as decreased dendritic complexity, dendritic spine density and percentage of mushroom shaped spines in hippocampal CA1 and dentate gyrus (DG) neurons. Furthermore, a significant reduction in Arc expression was detected upon BPA exposure. Strikingly, BPA exposure significantly increased the mIPSC amplitude without altering the mEPSC amplitude or frequency, accompanied by increased GABAARß2/3 on postsynaptic membrane in cultured CA1 neurons. In summary, our study indicated that Arc, together with the increased surface GABAARß2/3, contributed to BPA induced spatial memory deficits, providing a novel molecular basis for BPA achieved brain impairment.