Abstract. The chemotherapeutic approach using non-toxic natural products may be one of the strategies for the management of the cholangiocarcinoma. Here we report that in vitro treatment of human cholangiocarcinoma QBC939 cells with berberine, a naturally occurring isoquinoline alkaloid, decreased cell viability and induced cell death in a dose-dependent manner, which was associated with an increase in G1 arrest. Our western blot analysis showed that berberine-induced G1 cell cycle arrest was mediated through the increased expression of cyclin-dependent kinase inhibitors (Cdki) proteins (Cip1/p21 and Kip1/p27); a simultaneous decrease in Cdk2 and Cdk4 and cyclins D1, and reduced activity of the Cyclins-Cdk complex. In additional studies, treatment of QBC939 cells with different concentrations (10, 40, 80 μM) of berberine for 48 h resulted in a significant dose-dependent increase in apoptosis compared to the non-berberine-treated control, which was associated with an increased expression of pro-apoptotic protein Bax and decreased expression of anti-apoptotic proteins Bcl-2 and Bcl-xL. Together, this study for the first time identified berberine as a chemotherapeutic agent against human cholangiocarcinoma cells QBC939 cells in vitro. Further in vivo studies are required to determine whether berberine could be an effective chemotherapeutic agent for the management of cholangiocarcinoma.

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Oxybuprocaine and proxymetacaine were more potent at producing cutaneous anesthesia but were less potent than bupivacaine at producing central nervous system and cardiovascular toxicity.

and MMP-9 activities from its lowest concentration, and MMP-1 and MMP-2 at its higher concentrations, which implies a greater protective effect on elastin. It dramatically increased the expression of types I, III, and V collagens, and elastin, fibrillin-1, and fibrillin-2 in dermal fibroblasts. The effects were similar to those of ascorbic acid. This is the first report identifying xanthohumol's potential to improve skin structure and firmness: it simultaneously inhibits the activities of elastase/MMPs and stimulates the biosynthesis of fibrillar collagens, elastin, and fibrillins.pp. 133-145 Comparison of hydration, tyrosinase resistance, and antioxidant activation in three kinds of pearl powders by

The present study aimed to investigate the function of micro (mi)RNA-153 against isoflurane-induced neurotoxicity and its mechanism. In isoflurane-induced mice, miRNA-153 expression was downregulated compared with in the control group. Downregulation of miRNA-153 induced neurocyte apoptosis, reduced cell growth and promoted oxidative stress in an in vitro model. Overexpression of miRNA-153 reduced oxidative stress, promoted cell growth and inhibited neurocyte apoptosis within an in vitro model. Downregulation of miRNA-153 suppressed nuclear erythroid-2 related factor 2 (Nrf2)/antioxidant response element (ARE) signaling pathway, which was induced via the overexpression of miRNA-153 in vitro . The Nrf2 agonist, dimethyl fumarate (2.5 µM), induced the Nrf2/ARE signaling pathway and reduced oxidative stress to induce neurocyte apoptosis in vitro following treatment with anti-miRNA-153. The results of the present study suggested the function of miRNA-153 against neurotoxicity via Nrf2/ARE-mediated cytoprotection.