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AIM:To investigate the innate immune reactivity of tumor necrosis factor-alpha (TNF-α),Toll-like receptor 4 (TLR4),and CD14 in the liver of non-alcoholic steatohepatitis (NASH) model rats. 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 irnmunohistochemical investigation and RNA extraction.The liver specimens were immunostained for TNF-α,TLR4,and CD14.The gene expressions of TNF-α,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-αproduction. RESULTS:The serum and liver levels of TNF-αin the CDAA-fed rats increased significantly as compared with the control group,as did the immunohistochemical values and gene expressions of TNF-α,TLR4,and CD14 with the progression of steatohepatitis.TNF-αproduction from the isolated Kupffer cells of the CDAA- fed rats was elevated by lipopolysaccharide stimulation. CONCLUSION:The expressions of TNF-α,TLR4,and CD14 increased in the NASH model,suggesting that TLR4 and CD14-mediated endotoxin liver damage may also occur in NASH.
AIM: To investigate the innate immune reactivity of tumor necrosis factor-alpha (Toll-like receptor 4 (TLR4), and CD14 in the liver of non-alcoholic steatohepatitis (NASH) model rats. METHODS: Male F344 rats were fed a choline- deficient L-amino-acid-defined (CDAA) diet. These rats were killed after 4 or 8 wk of the diet, and their livers were removed for irnmunohistochemical investigation and RNA extraction. The liver specimens were immunostained for TNF -α, TLR4, and CD14. The gene expressions of TNF-α, 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-α production. RESULTS: The serum and liver levels of TNF-αin the CDAA-fed rats increased significantly compared to the control group, as did the immunohistochemical values and gene expressions of TNF-α, TLR4, and CD14 with the progression of steatohepatitis.TNF-αproduction from the isolated Kupffer cells of the CDAA-fed rats was elevated by lipopolysaccharide stimulation. CONCLUSION: The expressions of TNF-α, TLR4, and CD14 increased in the NASH model, suggesting that TLR4 and CD14-mediated endotoxin liver damage may also occur in NASH.