BACKGROUND： Sepsis has become the greatest threat to in-patients, with a mortality of over 25%.The dysfunction of gut barrier, especially the immunological barrier, plays an important role in the development of sepsi...BACKGROUND： Sepsis has become the greatest threat to in-patients, with a mortality of over 25%.The dysfunction of gut barrier, especially the immunological barrier, plays an important role in the development of sepsis. This dysfunction occurs after surgery, but the magnitude of change does not differentiate patients with sepsis from those without sepsis. Increased intestinal permeability before surgery is of no value in predicating sepsis. The present study aimed to observe the changes of intestinal mucosal immunologic barrier in rat models of sepsis induced by cecal ligation and puncture.METHODS： Sixty Sprague-Dawley rats were randomly divided into a sepsis group （n=45） and a control group （n=15）. The rats in the sepsis group were subjected to cecal ligation and puncture （CLP）, whereas the rats in the control group underwent a sham operation. The ileac mucosa and segments were harvested 3, 6 and 12 hours after CLP, and blood samples were collected. Pathological changes, protein levels of defensin-5 （RD-5） and trefoil factor-3 （TFF3） mRNA, and lymphocytes apoptosis in the intestinal mucosa were determined. In an additional experiment, the gut-origin bacterial DNA in blood was detected.RESULTS： The intestinal mucosa showed marked injury with loss of ileal villi, desquamation of epithelium, detachment of lamina propria, hemorrhage and ulceration in the sepsis group. The expression of TFF3 mRNA and level of RD-5 protein were decreased and the apoptosis of mucosal lymphocyte increased （P〈0.05） in the sepsis group compared with the control group. Significant differences were observed in RD-5 and TFF3 mRNA 3 hours after CLP and they were progressively increased 6 and 12 hours after CLP in the sepsis group compared with the control group （P〈0.05, RD-5 F=11.76, TFF3 F=16.86 and apoptosis F=122.52）. In addition, the gut-origin bacterial DNA detected in plasma was positive in the sepsis group.CONCLUSION： The immunological function of the intestinal mucosa was impaired in septic rats 展开更多
BACKGROUND：As the regulators of cytokines, suppressors of cytokine signaling （SOCS） play an important role in the inflammation reaction. Some studies found that SOCS-1 and SOCS-3 were involved in the pathogenesis o...BACKGROUND：As the regulators of cytokines, suppressors of cytokine signaling （SOCS） play an important role in the inflammation reaction. Some studies found that SOCS-1 and SOCS-3 were involved in the pathogenesis of some inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease. But the expressions of SOCS in coronary heart disease have not yet been reported. This study aimed to investigate the expression and clinical significance of SOCS-1 and SOCS-3 in the myocardium of patients with sudden cardiac death （SCD）.METHODS： Myocardial autopsy specimens were collected from 24 patients at the Forensic Medicine Department of Sun Yat-Sen University, Guangzhou, China between 2005 and 2006. Of them, 9 patients had autopsy findings consistent with coronary atherosclerosis （non-myocardial infarction） leading to SCD （non-MI group）, 7 died of acute myocardial infaction （MI group）, and 8 died from traffic accidents and trauma （control group）. The expressions of SOCS-1 mRNA and SOCS-3 mRNA in the myocardium of the non-MI, MI and control groups were detected using RT-PCR. The levels of SOCS-1 and SOCS-3 proteins were detected using immunohistochemistry. Statistical analyses were performed using SPSS version 13.0 sottware and the data were analyzed by ANOVA.RESULTS： The expressions of SOCS-1 mRNA and SOCS-3 mRNA in the non-MI and MI groups were significantly higher than those in the control group[（0.788±0.101）, （0.741±0.111） vs. （0.436±0.044）, （P〈0.01）; （0.841±0.092）, （0.776±0.070） vs. （0.454±0.076）, （P〈0.01）] respectively. The antibody-positive cells of SOCS-1 protein in the myocardium of the non-MI and MI groups were significantly higher than those in the myocardium of the control group[（320.00±48.48）, （347.14±70.88） vs. （42.50±10.35）, （P〈0.01）] respectively. The antibody-positive cells of SOCS-3 protein in the myocardium of the non-MI and MI groups were significantly higher than those in the myocardium of the contr展开更多
基金This study was supported by the National Natural Science Foundation of Guangdong Province （06021323）.
文摘BACKGROUND： Sepsis has become the greatest threat to in-patients, with a mortality of over 25%.The dysfunction of gut barrier, especially the immunological barrier, plays an important role in the development of sepsis. This dysfunction occurs after surgery, but the magnitude of change does not differentiate patients with sepsis from those without sepsis. Increased intestinal permeability before surgery is of no value in predicating sepsis. The present study aimed to observe the changes of intestinal mucosal immunologic barrier in rat models of sepsis induced by cecal ligation and puncture.METHODS： Sixty Sprague-Dawley rats were randomly divided into a sepsis group （n=45） and a control group （n=15）. The rats in the sepsis group were subjected to cecal ligation and puncture （CLP）, whereas the rats in the control group underwent a sham operation. The ileac mucosa and segments were harvested 3, 6 and 12 hours after CLP, and blood samples were collected. Pathological changes, protein levels of defensin-5 （RD-5） and trefoil factor-3 （TFF3） mRNA, and lymphocytes apoptosis in the intestinal mucosa were determined. In an additional experiment, the gut-origin bacterial DNA in blood was detected.RESULTS： The intestinal mucosa showed marked injury with loss of ileal villi, desquamation of epithelium, detachment of lamina propria, hemorrhage and ulceration in the sepsis group. The expression of TFF3 mRNA and level of RD-5 protein were decreased and the apoptosis of mucosal lymphocyte increased （P〈0.05） in the sepsis group compared with the control group. Significant differences were observed in RD-5 and TFF3 mRNA 3 hours after CLP and they were progressively increased 6 and 12 hours after CLP in the sepsis group compared with the control group （P〈0.05, RD-5 F=11.76, TFF3 F=16.86 and apoptosis F=122.52）. In addition, the gut-origin bacterial DNA detected in plasma was positive in the sepsis group.CONCLUSION： The immunological function of the intestinal mucosa was impaired in septic rats
文摘BACKGROUND：As the regulators of cytokines, suppressors of cytokine signaling （SOCS） play an important role in the inflammation reaction. Some studies found that SOCS-1 and SOCS-3 were involved in the pathogenesis of some inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease. But the expressions of SOCS in coronary heart disease have not yet been reported. This study aimed to investigate the expression and clinical significance of SOCS-1 and SOCS-3 in the myocardium of patients with sudden cardiac death （SCD）.METHODS： Myocardial autopsy specimens were collected from 24 patients at the Forensic Medicine Department of Sun Yat-Sen University, Guangzhou, China between 2005 and 2006. Of them, 9 patients had autopsy findings consistent with coronary atherosclerosis （non-myocardial infarction） leading to SCD （non-MI group）, 7 died of acute myocardial infaction （MI group）, and 8 died from traffic accidents and trauma （control group）. The expressions of SOCS-1 mRNA and SOCS-3 mRNA in the myocardium of the non-MI, MI and control groups were detected using RT-PCR. The levels of SOCS-1 and SOCS-3 proteins were detected using immunohistochemistry. Statistical analyses were performed using SPSS version 13.0 sottware and the data were analyzed by ANOVA.RESULTS： The expressions of SOCS-1 mRNA and SOCS-3 mRNA in the non-MI and MI groups were significantly higher than those in the control group[（0.788±0.101）, （0.741±0.111） vs. （0.436±0.044）, （P〈0.01）; （0.841±0.092）, （0.776±0.070） vs. （0.454±0.076）, （P〈0.01）] respectively. The antibody-positive cells of SOCS-1 protein in the myocardium of the non-MI and MI groups were significantly higher than those in the myocardium of the control group[（320.00±48.48）, （347.14±70.88） vs. （42.50±10.35）, （P〈0.01）] respectively. The antibody-positive cells of SOCS-3 protein in the myocardium of the non-MI and MI groups were significantly higher than those in the myocardium of the contr
