Innate immune reactivity of the liver in rats fed a choline-deficient L-amino-acid-defined diet

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 cholinedeficient 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-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-~ in 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-α production from the isolated Kupffer cells of the CDAAfed rats was elevated by lipopolysaccharide stimulation. CONCLUSION： The expressions of TNF-α, TLR4, and CD14 increased in the NASH model, suggesting that

瞄准：调查肿瘤坏死 factor-alpha (TNF-alpha ) 的天生的有免疫力的反应，像使用费的受体 4 (TLR4 ) ，并且在非酒精的 steatohepatitis (NASH ) 的肝的 CD14 为老鼠建模。方法：男 F344 老鼠被喂一本胆碱缺乏的 L-amino-acid-defined (CDAA ) 食谱。老鼠在食谱的 4 或 8 wk 以后被打死，并且他们的肝为免疫被移开组织化学的调查和 RNA 抽取。肝标本是为 TNF-alpha， TLR4，和 CD14 染色的免疫。TNF-alpha， TLR4，和 CD14 的基因表情被 reverse-transcriptase 聚合酶链反应(RT-PCR ) 决定。Kupffer 房间被 Percoll 坡度远心沉淀从肝孤立，并且当时是有教养的测量 TNF-alpha 生产。结果：在老鼠作为与控制相比显著地增加了的 CDAA-fed 的 TNF-alpha 的浆液和肝层次组织，，与 steatohepatitis 的前进做了免疫组织化学的值和 TNF-alpha， TLR4，和 CD14 的基因表达式。从 CDAA-fed 老鼠的孤立的 Kupffer 房间的 TNF-alpha 生产被脂肪的多糖刺激提高。结论：TNF-alpha， TLR4，和 CD14 的表情在 NASH 模型增加了，建议 TLR4 和调停 CD14 的内毒素肝损坏可以也发生在 NASH。