【摘要】 目的研究大鼠肝移植缺血再灌注后Kupffer细胞CD14和Toll样受体4(TLR4)的表达及其参与缺血再灌注损伤的机制。方法建立肝移植缺血再灌注模型,并分为正常对照组、缺血再灌注组、抗CD14抗体组,每组均为10只大鼠。分离培养大鼠肝移植缺血再灌注后的Kupffer细胞。检测Kupffer细胞CD14及TLR4的mRNA、蛋白表达、核转录因子κB(NFκB)活性以及培养上清TNFα的分泌量。结果再灌注后Kupffer细胞CD14及TLR4的mRNA和蛋白表达明显高于正常对照组(P<001),再灌注后核转录因子κB活性、培养上清TNFα表达量明显高于对照组(P<001)。用抗CD14抗体后NFκB活性,TNFα表达量明显下降(与再灌注组相比,P<005),但仍然高于对照组(P<001)。结论缺血再灌注后肠道内毒素(脂多糖)能够上调Kupffer细胞CD14及TLR4的表达,激活NFκB,启动细胞因子的转录和分泌,但除CD14和TLR4以外的其他信号途径参与了缺血再灌注损伤。更多还原

【Abstract】 Objective To study the expression of lipopolysaccharide（LPS） receptor CD14 and Toll-like receptor 4 （TLR4） on Kupffer cells and its role in ischemia-reperfusion injury （IRI） on rat liver graft. Methods The Kupffer cells following IRI were isolated and divided into control, ischemia-reperfusion （IR）, and anti-CD14 antibody group. The mRNA and protein expression of CD14 and TLR4, nuclear factor kappa B （NF-κB） activity and TNF-α level in supernatant were measured. Results The mRNA and protein expression of CD14 and TLR4 in IR group were significantly higher than those in control group^P<0.01. The NF-κB activity and TNF-α level in IR group were significantly higher than those in control group（P<0.01）, and they greatly decreased after anti CD14 antibody treatment （compared with IR group, P<0.05）, but were still significantly higher than those in control group（P<0.01）. Conclusions LPS following IRI could up-regulate CD14 and TLR4 gene and protein expression on Kupffer cells, and subsequently activate NF-κB to produce cytokines, but other signal transduction pathways might also participate in the IRI.更多还原