Publications (2)2.61 Total impact
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ABSTRACT: Our objective was to investigate the expression of scavenger receptor (SR) and CD14 in the liver and their relationship with local anti-inflammatory and proinflammatory responses in endotoxemia in order to uncover the mechanism for the liver to turn into effector organ from defense one at the level of cell receptors in sepsis. Mouse models of endotoxemia of different severity were reproduced by injection of different doses of lipopolysaccharide (LPS) via tail vein. Expression of SR and CD14 in the liver was assayed by immunohistochemistry and was then analyzed with an image analysis system. The levels of TNFalpha, IL-6, IL-4, and IL-10 in liver tissue were determined with ELISA. Expression of SR in the liver in the high-dose group was markedly decreased 1 h after injection of LPS, and also in low- and medium-dose groups at 3 h. The expression of SR in the liver in the three groups was shown to be progressively decreased with the time prolonged. There was significant difference in average optical density (OD) values of SR among the three groups. The expression of CD14 in the liver in the three groups was shown to be significantly increased 1 h after injection of LPS, and much more with the time prolonged. But there was no significant difference in OD values of CD14 among the three groups. The contents of intrahepatic proinflammatory mediators TNFalpha and IL-6 and anti-inflammatory mediators IL-4 and IL-10 were successively significantly increased after injection of LPS. The release of anti-inflammatory mediators was shown to be later than that of proinflammatory mediators. Correlation analysis indicated that there was negative correlation between expression of SR and CD14, and that changes of TNFalpha, IL-6, IL-4, and IL-10 levels in liver tissues were correlated significantly positively with OD values of CD14 and negatively with OD values of SR. Expression of SR in the liver was shown to be progressively decreased, and that of CD14 increased in endotoxemia, which was closely related to the uncontrolled inflammatory response in liver. This might be an important mechanism for the liver to turn into effector organ from defense one in sepsis.Shock 08/2001; 16(1):75-80. · 2.61 Impact Factor
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ABSTRACT: To investigate the protective effects of BPI on the vital organ function after endotoxic shock in rats, and to provide experimental evidence for further clinical studies. 12.5 mg/kg of E. coli 026:B6 LPS were bolus injected via i.a. to reproduce endotoxic shock. Immediately after injection of LPS, 5 mg/kg of BPI or equal volume of physiological saline were bolus injected via i.a. The survival time of shocked animals was prolonged in the BPI group, 24 h survival rate was higher than that in the saline group. The values of mean arterial pressure, left intraventricular systolic pressure, isovolemic ventricular pressure, and dp/dtmax in the BPI group were markedly higher than those in the saline group. The plasma glutamic-pyruvic transaminase and urea nitrogen levels were obviously lower than those in the saline group. The plasma endotoxin and TNF levels in the BPI group were significantly lower than those in the saline group. BPI has good protective effects on cardiac, hepatic, and renal function in endotoxic shock in rats, indicating that BPI might be useful in clinic treatment of sepsis/septic shock.Zhonghua wai ke za zhi [Chinese journal of surgery] 03/1999; 37(2):120-2.