scholarly journals Localization of HBx antigen in the liver tissues from patients with chronic hepatitis B.

Kanzo ◽  
1991 ◽  
Vol 32 (7) ◽  
pp. 675-682
Author(s):  
Akira FURUKATA ◽  
Mitsuhiko MORIYAMA ◽  
Yasuyuki ARAKAWA ◽  
Yutaka MATSUO ◽  
Noboru YANAIHARA
1996 ◽  
Vol 24 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Kiyoshi Mochizuki ◽  
Norio Hayashi ◽  
Naoki Hiramatsu ◽  
Kazuhiro Katayama ◽  
Yuko Kawanishi ◽  
...  

2013 ◽  
Vol 21 (14) ◽  
pp. 1321
Author(s):  
Zhan-Qing Zhang ◽  
Wei Lu ◽  
Yan-Bing Wang ◽  
Xiao-Fang Jia ◽  
Li-Jun Zhang ◽  
...  

2016 ◽  
Vol 235 ◽  
pp. 92-98 ◽  
Author(s):  
Zhan-Qing Zhang ◽  
Wei Lu ◽  
Yan-Bing Wang ◽  
Qi-Cheng Weng ◽  
Zhi-Yong Zhang ◽  
...  

2004 ◽  
Vol 10 (3) ◽  
pp. 385 ◽  
Author(s):  
Song-Mei Lou ◽  
You-Ming Li ◽  
Kai-Ming Wang ◽  
Wei-Min Cai ◽  
Hong-Lei Weng

2008 ◽  
Vol 14 (4) ◽  
pp. 607 ◽  
Author(s):  
Zhi-Xin Zhao ◽  
Qing-Xian Cai ◽  
Xiao-Mou Peng ◽  
Yu-Tian Chong ◽  
Zhi-Liang Gao

2008 ◽  
Vol 31 (3) ◽  
pp. 123 ◽  
Author(s):  
Xiu-Qing Wei ◽  
Yun-Wei Guo ◽  
Jia-Jun Liu ◽  
Zhuo-Fu Wen ◽  
Shao-Ji Yang ◽  
...  

Purpose: To investigate the importance of Toll-like receptor 4 (TLR4) expression on hepatocytes obtained from Chronic Hepatitis B patients as well as on hepatocellular carcinoma HepG2 and HepG2.2.15 cell lines. Methods: Expression of TLR4 in liver tissues was determined by immunohistochemistry in 75 patients with CHB and in10 healthy controls. The protein and mRNA 1eve1s of TLR4 in hepatocellular carcinoma HepG2 and HepG2.2.15 cells were measured by flow cytometry (FCM) and real-time quantitative PCR (RQ-PCR), and endotoxin triggered TNF-? secretion in HepG2 and HepG2.2.15 cells was evaluated by ELISA. Results: TLR4 expressed mainly in the cytoplasm and some on cell membrane in hepatocytes. The staining scores of TLR4 expression in the liver tissues of patients with CHB were significantly higher than that of healthy controls. The liver tissues from patients with severe CHB expressed higher level of TLR4 than those from patients with mild CHB. Furthermore, the staining scores of TLR4 expression in the liver tissues of patients with CHB were positively correlated with the grading scores. Our results also showed that the mean fluorescence intensity and TNF-? secretion induced by endotoxin as well as the protein and mRNA 1eve1s of TLR4 in HepG2.2.15 cells were all significantly higher than those in HepG2 cells. Conclusion: TLR4 was up-regulated in the hepatocytes in patients with CHB. This indicates a potentially important interaction between TLR4 expression and the pathogenesis of CHB.


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