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Induction of acute hepatic injury by endotoxin in mice 被引量:3

Induction of acute hepatic injury by endotoxin in mice
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摘要 Objective: To investigate the changes of scavenger re-ceptor (SR) and CD<sub>14</sub> in Kupffer cells in endotox-emia in order to uncover the mechanism of the liverto turn a defense organ into effector one in sepsis.Methods: Mouse models of endotoxemia of differentseverity were reproduced by injection of different do-ses of lipopolysaccharide (LPS) via the tail vein.The expression of SR and CD<sub>14</sub> in the liver was as-sayed by immunohistochemistry and was subsequent-ly analyzed with an image analysis system. The levelsof TNF-α and IL-6 in liver tissue were determinedwith ELISA.Results: The expression of SR in the liver in the high-dose group was markedly decreased one hour afterinjection of LPS, and also in the low-dose group at 3hours. The expression of SR in the liver in the twogroups was shown to be progressively decreased withthe time prolonged. There was significant differencein average optical density (OD) values of SR be-tween the two groups. The expression of CD<sub>14</sub> in thetwo groups was shown to be significantly increasedone hour after injection of LPS, and more signifi-cantly with the time prolonged. But there was no sig-nificant difference in OD values of CD<sub>14</sub> between thetwo groups. The contents of intrahepatic proinflam-matory mediators TNF-α, IL-6, ALT and TBILwere significantly increased after injection of LPS.Correlation analysis revealed that the changes ofTNF-α, IL-6, ALT, and TBIL were negatively cor-related with the expression of SR, and positively withthe expression of CD<sub>14</sub>.Conclusion: The up-regnlation of CD<sub>14</sub> expressionand down-regulation of SR expression on Kupffercells might be one of the important mechanisms forthe conversion of Kupffer cells from immune defen-sive to inflammatory response cells in acute hepaticinjury.
出处 《Hepatobiliary & Pancreatic Diseases International》 SCIE CAS 2002年第4期558-564,共7页 国际肝胆胰疾病杂志(英文版)
基金 This work is supported by a grant from the National Natural Science Foundation of China (No. 39770313).
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参考文献17

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二级参考文献5

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