Objective To study the effect of chronic poisoning of ketamine on brain cell apoptosis in adult mouse under different duration and doses. Methods The mouse model of chronic poisoning of ketamine was established on adult mouse by tail vein injection of ketamine twice every week with different doses (4, 10, 20 and 30 m g/kg). The mice were sacrificed after continuous injection of ketamine of 1, 2, 4, 8 and 12 weeks. The qualitative assessment of apoptosis was made by transmission electron microscope and the quantitative assessment was made by Caspase-3 im m umofluorescence staining method and terminal deoxynucleotidyl transferase-mediated dU TP nick end labeling (TUNEL ) to estimate the time point of apoptosis. All the experimental results were statistically analyzed. Results The neuron apoptosis was ob-served in hippocam pus and corpus striatum by transmission electron microscope one week after adminis-tration, and continued for eight weeks. High level of Caspase-3 expression was observed one week after administration, but with a lowlevel expression after 4 weeks. The num ber of TUNEL positive cells ob-viously increased one week after administration and maintained in ahigh num ber at 4 weeks. Conclu-sion Ketamine by tail vein injection could induce neuron apoptosis in adult mouse.

Liver sinusoidal endothelial cells (LSECs) are the highest proportion of liver non-parenchymal cells with fenestrae structure and high endocytic ability maintaining liver homeostasis and playing an indispensable role in the physiology and patholo-gy of the liver.LSECs are involved in the regulation of patholog-ical process in nonalcoholic fatty liver disease(NAFLD),alco-holic fatty liver(AFL),hepatocellular carcinoma(HCC),liverregeneration and liver fibrosis mainly via antiinflammation,endocytosis,secretion of angiocrine signals and maintaining thequiescence phenotype of HSCs.This review highlights the physiological function of LSECs and the different roles in different pathological conditions,which aims to provide a new perspectivefor the treatment of liver diseases through targeting LSECs.

Nicotinamide adenine dinucleotide phosphate oxidase ( NOXs) contributes to the production of reactive oxygen species ( ROS) in liver fibrosis, resulting in the activation of endoplas-mic reticulum stress ( ERS ) and IRE1α-XBP1 signaling path-way. ROS is a series of oxygen metabolites and its derivatives, produced by the single electron reduction of molecular oxygen ( O2 ) , including superoxide anion ( O2- ) , hydroxyl radical (-OH) , hydrogen peroxide ( H2 O2 ) , hypochlorite ion ( OCl-) and so on. They can interact with a large number of molecules, including small inorganic molecules, proteins, lipids, carbohy-drates and nucleic acids, resulting in lipid peroxidation of cell damaging molecules. And as a second messenger, ROS can also affect the proliferation and activation of HSC in liver fibrosis, and induce the hepatocyte apoptosis through a variety of cellular signal transduction. Here we review the current status of the study on the mechanism of NOXs in liver fibrosis.