Abstract | AIM: METHODS: Male F344 rats were fed a choline-deficient L- amino-acid-defined ( CDAA) diet. The rats were killed after 4 or 8 wk of the diet, and their livers were removed for immunohistochemical investigation and RNA extraction. The liver specimens were immunostained for TNF-alpha, TLR4, and CD14. The gene expressions of TNF-alpha, TLR4, and CD14 were determined by reverse-transcriptase polymerase chain reaction (RT-PCR). Kupffer cells were isolated from the liver by Percoll gradient centrifugation, and were then cultured to measure TNF-alpha production. RESULTS: The serum and liver levels of TNF-alpha in the CDAA-fed rats increased significantly as compared with the control group, as did the immunohistochemical values and gene expressions of TNF-alpha, TLR4, and CD14 with the progression of steatohepatitis. TNF-alpha production from the isolated Kupffer cells of the CDAA-fed rats was elevated by lipopolysaccharide stimulation. CONCLUSION: The expressions of TNF-alpha, TLR4, and CD14 increased in the NASH model, suggesting that TLR4 and CD14-mediated endotoxin liver damage may also occur in NASH.
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Authors | Hideto Kawaratani, Tatsuhiro Tsujimoto, Toshiyuki Kitazawa, Mitsuteru Kitade, Hitoshi Yoshiji, Masahito Uemura, Hiroshi Fukui |
Journal | World journal of gastroenterology
(World J Gastroenterol)
Vol. 14
Issue 43
Pg. 6655-61
(Nov 21 2008)
ISSN: 1007-9327 [Print] United States |
PMID | 19034968
(Publication Type: Journal Article)
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Chemical References |
- Amino Acids
- Lipopolysaccharide Receptors
- Tlr4 protein, rat
- Toll-Like Receptor 4
- Tumor Necrosis Factor-alpha
- Alanine Transaminase
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Topics |
- Alanine Transaminase
(blood)
- Amino Acids
(adverse effects)
- Animals
- Cells, Cultured
- Choline Deficiency
(complications)
- Disease Models, Animal
- Fatty Liver
(etiology, metabolism, pathology)
- Immunity, Innate
(physiology)
- Kupffer Cells
(metabolism, pathology)
- Lipopolysaccharide Receptors
(metabolism)
- Liver
(metabolism, pathology)
- Male
- Rats
- Rats, Inbred F344
- Toll-Like Receptor 4
(metabolism)
- Tumor Necrosis Factor-alpha
(metabolism)
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