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Ren-wen Zhang, Yong Qiao, Xiao-hua Hao, Hong-min Li, Hui Ren, Xiao-jing Zhang, Hong-shan Wei and Xiao-yuan Xu

growth factor-β signaling in hepatocytes promotes hepatic fibrosis and carcinogenesis in mice with hepatocyte-specific deletion of TAK1. Gastroenterology 2013; 144(5):1042-1054. 17. Friedman SL. Mechanisms of hepatic fibrogenesis. Gastroenterology 2008; 134(6):1655-1669. 18. Friedman SL. Hepatic stellate cells: protean, multifunctional, and enigmatic cells of the liver. Physiol Rev 2008; 88(1):125-172. 19. Amann T, Bataille F, Spruss T, Mühlbauer M, Gäbele E, Schölmerich J, et al. Activated hepatic stellate cells promote

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Kateřina Lněničková, Lenka Skálová, Lucie Stuchlíková, Barbora Szotáková and Petra Matoušková

, J. C. Wr andebe S. O. Mueller, Use of mRNA expression to detect the induction of drug metabolising enzymes in rat and human hepatocytes, Toxicol. Appl. Pharmacol. 235 (2009) 86-96; J. Skorkovská 1.019, V. Hanušová, V. Tománková, E. Anzenbacherová, B. Lišková, P. Anzenbacher 5. P. Matoušková, H. Bártíková, I. Boušová, B. Szotáková, J. Martin, and L. Skálová, Effect of defined green tea extract in various dosage schemes on drug-metabolizing enzymes in mice in vivo, J. Funct. Foods 10 (2014) 327-335; https

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Ge Bai, Hui Li, Yansong Ge, Qianzhen Zhang, Jiantao Zhang, Mingzi Chen, Tao Liu and Hongbin Wang

neutrophils, which further contribute to cellular injury and cell death (necrosis or apoptosis). Following hepatic ischaemia-reperfusion, large amounts of reactive oxygen species (ROS) are produced by the xanthine oxidase system, macrophage system, and mitochondrial respiratory chain ( 11 ). Moreover, the release of ROS can damage proteins, nucleic acids, cell membranes, and lipids ( 30 ), which can directly damage the hepatocytes. Autophagy has also been reported to be related to hepatic ischaemia-reperfusion injury. Hepatocytes in thus injured liver degrade damaged and

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Lidia Radko, Maria Minta and Sylwia Stypuła-Trębas

References 1. Baliharová V., Skálova L., Maas R.F.M., De Vrieze G., Bull S., Fink-Gremmels J.: The effects of benzimidazole anthelmintics on P4501A in rat hepatocytes and HepG2 cells. Res Vet Sci 2003, 75, 61-69. 2. Blaauboer B.J., Boobis A.R., Castell J.V., Coecke S., Groothuis G.M.M., Guillouzo A., Hall T.J., Hawksworth G.M. Lorenzon G., Miltenburger H.G., Rogiers V., Skett P., Viia P., Wiebel F.J.: The practical applicability of hepatocyte cultures in routine testing. ECVAM Workshop Report 1. ATLA 1994, 22, 231

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Agnieszka Pedrycz, Zbigniew Boratyński, Marcin Orłowski and Piotr Siermontowski

. Thorac Cardiovasc Surg 1999, 118, 655-664. 12. Mukhopadhyay I., Nazir A., Saxena D.K., Chowdhuri D.K.: Toxicity of cypermethrin: HSp70 as a biomarker of response in transgenic Drosophila . Biomarkers 2002, 7, 501-510. 13. Pedrycz A., Kot K., Olesiński I.: Immunohistochemical evaluation of caspase 3 expression in rats' hepatocytes after L-arginine therapy. Bull Vet Inst Pulawy 2010, 54 , 101-103. 14. Rolye J.S., Ross J.A., Ansell I., Bollina P., Tulloch D.N., Habib F.K.: Nitric oxide donating nonsteroidal anti

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Hasan Turkez and Fatime Geyikoglu

;74:613-6. National Research Council. Guide for the Care and Use of Laboratory Animals. Washington (DC): National Academy Press; 1996. Wang HX, Ma XC, Deng QL. Cytotoxicity of flutamide and 2-hydroxyflutamide and their effects on CYP1A2 mRNA in primary rat hepatocytes. Acta Pharmacol Sin 2002;23:562-6. Rakba N, Melhaoui A, Loyer P, Delcros JG, Morel I, Lescoat G. Bgugaine, a pyrrolidine alkaloid from Arisarum vulgare , is a strong hepatotoxin in rat and human liver cell cultures. Toxicol Lett 1999

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Gang Lin, Xiaoyan Duan, Xiaobo Cai, Liyan Tian, Zhengjie Xu and Jiangao Fan


Background: Non-alcoholic fatty liver disease is considered a hepatic manifestation of the metabolic syndrome. It is associated with endothelial dysfunction as an early event of generalized atherosclerosis. However, it is unclear whether steatotic hepatocytes influence endothelial function directly. Objective: Explore the influence of hepatocyte steatosis on the function of endothelial cells. Methods: Oleic and palmitic acid (2:1 mixture, final concentration: 1 mM for 24 hours) was used to induce a normal adult hepatocyte strain (L-02) for transformation into steatosis cells. This was followed by oil red O staining and transmission electron microscopy (TEM) for verification. The culture solution of steatotic L-02 cells was filtered and collected, and added into the culture substrate of human umbilical vein endothelial cells (HUVECs). The expression of vascular cellular adhesion molecule -1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and E-selectin in HUVECs was detected by real-time polymerase chain reaction and Western blot assays. The apoptosis and proliferation of HUVECs was determined using flow cytometry. The experimental results were compared with the controls. Results: Oil red O staining and microscopic observation showed that the cytoplasm of induced L-02 cells contained a large amount of red lipid droplets. TEM results showed that the cytoplasm had lipid accumulation, swelling mitochondria, fewer cristae, and reduced number of rough endoplasmic reticula accompanied with degranulation. However, these changes were not observed in normal L-02 cells. As to the group of HUVECs treated by the filtrate of steatosis L-02 cells, the mRNA and protein expression of VCAM-1, ICAM-1, and E-selectin was higher than that in the control group. The difference was statistically significant (p <0.01). No significant difference was found when HUVECs apoptosis and proliferation were assessed by flow cytometry. Conclusion: Secretion from steatotic hepatocytes could boost the expression of VCAM-1, ICAM-1, and E-selectin in endothelial cells, indicating that hepatocyte steatosis could induce endothelial cell dysfunction. The proliferation and apoptosis of endothelial cells did not change, suggesting that hepatocyte steatosis had no influence on the viability of endothelial cells under this condition.

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Jun Cheng, Min Quan, Min Li, Shun-ai Liu and Qi Wang

hepatocytes. J Hepatol 2006;44:842-847. 26 Protzer U, Seyfried S, Quasdorff M, Sass G, Svorcova M, Webb D, et al. Antiviral activity and hepatoprotection by heme oxygenase-1 in hepatitis B virus infection. Gastroenterology 2007;133:1156-1165. 27 Levrero M, Pollicino T, Petersen J, Belloni L, Raimondo G, Dandri M. Control of cccDNA function in hepatitis B virus infection. J Hepatol 2009;51:581-592. 28 Belloni L, Pollicino T, De Nicola F, Guerrieri F, Raffa G, Fanciulli M, et al. Nuclear HBx binds the HBV minichromosome and

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Qing He, Qi-yuan Tang, Xiao-hua Le, De-liang Lv, Xiang-mei Zhang, Fei-jian Ao, Yi-min Tang, Shan Huang, John Nunnari and Gui-lin Yang

hepatitis B virus infection. Hepatology 1982;2:557-561. 4 Chu CM, LiawYF. Intrahepatic distribution of hepatitis B surface and core antigens in chronic hepatitis B virus infection: hepatocyte with cytoplasmic/membranous hepatitis B core antigen as a possible target for immune hepatocytolysis. Gastroenterology 1987;92:220-225. 5 Gudat F, Bianchi L, Sonnabend W, Thiel G, Aenishaenslin W, Stadler GA. Pattern of core and surface expression in liver tissue reflects state of specific immune response in hepatitis B. Lab Invest 1975

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Muyao Zhang, Xing Wei and Zhenfei Wang

every year [ 4 ]. Therefore, it is extremely important to study the mechanism of promotion of initiation and progression of hepatoma by HBV. HBx protein is one of the products of the HBV genome. Recent studies have found that HBx protein has great effects on the biological behaviors of hepatocytes and hepatoma cells, and that it plays important roles in promoting the initiation and progression of hepatoma, thus holding promise to becoming a new molecular target in hepatocellular carcinoma (HCC) therapy. 2 HBx protein The X protein (HBx) encoded by the X region