inducing resuscitation with herbal aromatics is important to modulate the brain intake of drugs in traditional Chinese medicine,but limited information has been available on the mechanism of action.The MDCK-MDRl monolayer is an excellent in vitro cell model to use as a tool to study blood brain barrier（BBB） screening.In this study,we established MDCK-MDR1 cell line by stable transfection and investigated the effects of several important herbal aromatics on BBB permeability.The characterization experiment demonstrated the MDCK-MDRl used in this study was valid.In a transport study,we found several herbal aromatics increased the permeability of fluorescein isothiocyanate-labeled dextran 4kDa（FD4） and inhibited efflux of Rhodaminel23（Rhol23）.These results demonstrated that herbal aromatics enhanced the BBB permeation of drugs by both inhibition of P-gp and opening of the BBB tight junction,thus providing new insights for understanding the mechanisms of aromatic compounds＇ BBB permeability.
Gd3＋ complexes have a variety of medical applications.In order to shed light on the mechanism of hepatotoxicity of Gd3＋ compounds,we investigated the effects of GdCl3 on human embryo liver cell strand （L02 cells）.The experimental results showed that long-time exposure to GdCl3 resulted in L02 cell apoptosis.The incubation of L02 cells with GdCl3 first induced increase in cellular reactive oxygen species （ROS） and decrease in mitochondrial inner membrane potential （？ψm）.It later resulted in the activation of poly （ADP-ribose） polymerase （PARP） and the release of mitochondrial apoptosis-inducing factor （AIF）.The activation of caspase 3,however,was not observed.Antioxidants could significantly reduce GdCl3-induced decrease of Δψm,release of AIF,and cell apoptosis.Although GdCl3 caused a significant increase in cell membrane permeability in L02,the change of cell membrane permeability was unlikely to be involved in GdCl3-induced cell apoptosis.Overall,our experimental results suggested that GdCl3 induced apoptosis of human embryo liver L02 cell line by ROS-mediated AIF pathway.
