AIM： To investigate the role of CXCL16 in the pathogenesis of immunological liver injury and to explore the possible mechanism ofT lymphocyte infiltration regulated by CXCL16. METHODS： Immunological liver injury in ...AIM： To investigate the role of CXCL16 in the pathogenesis of immunological liver injury and to explore the possible mechanism ofT lymphocyte infiltration regulated by CXCL16. METHODS： Immunological liver injury in murine model was induced by Bacille Calmette-Guerin and lipopolysaccharide. Expression pattern and distribution of CXCL16 were examined by real-time quantitative RT-PCR and immunohistochemical analysis. Anti-CXCL16 antibody was administrated in vivo to investigate its effect on T-cell recruitment and acute hepatic necrosis. The survival of murine model was also evaluated. RESULTS, The murine immunological liver injury model was successfully established, CXCL16 expression increased and predominantly distributed in periportal areas and vascular endothelia in injured liver tissues. Administration of anti-CXCL16 Ab protected the mice from death and acute liver damage. Approximately 70% of the mice survived for 72 h in the anti-CXCL16 Ab treatment group, whereas 80% died within 72 h in control Ab group. The number of liver-infiltrating T lymphocytes was significantly reduced from 1.01×10^7 to 3.52×10^6/liver, compared with control Ab treatment. CONCLUSION： CXCL16 is involved in immunological liver injury by regulating T lymphocyte infiltration in liver tissue.展开更多
AIM： To evaluate the protective effects of preconditioning by α-lipoic acid （LA） in patients undergoing hepatic resection under inflow occlusion of the liver. METHODS： Twenty-four patients undergoing liver resect...AIM： To evaluate the protective effects of preconditioning by α-lipoic acid （LA） in patients undergoing hepatic resection under inflow occlusion of the liver. METHODS： Twenty-four patients undergoing liver resection for various reasons either received 600 mg LA or NaCI 15 min before transection performed under inflow occlusion of the liver. Blood samples and liver wedge biopsy samples were obtained after opening of the abdomen immediately after inflow occlusion of the liver, and 30 min after the end of inflow occlusion of the liver. RESULTS： Serum levels of aspartate transferase and alanine transferase were reduced at all time points in patients who received LA in comparison to those who received NaCL. This was accompanied by reduced histomorphological features of oncosis. We observed TUNEL-positive hepatocytes in the livers of the untreated patients, especially after 30 min of ischemia. LA attenuated this increase of TUNEL-positive hepatocytes. Under preconditioning with LA, ATP content was significantly enhanced after 30 min of ischemia and after 30 min of reperfusion. CONCLUSION： This is the first report on the potential for LA reducing ischemia/reperfusion injury （IRI） of the liver in humans who were undergoing liver surgery. Beside its simple and rapid application, side effects did not occur. LA might therefore represent a new strategy against hepatic IRI in humans.展开更多
Objective: To investigate the histopathological changes in the liver and other organs after impact injury. Methods: The rabbits were impacted with a BIM IV biological impacting machine at the xiphoid process. The seve...Objective: To investigate the histopathological changes in the liver and other organs after impact injury. Methods: The rabbits were impacted with a BIM IV biological impacting machine at the xiphoid process. The severity of liver injury was graded and scored through gross anatomy. At the same time, the pathological changes in the liver, heart, and lung were observed by light and electron microscopes. Results: Light microscopy showed that the pathological changes in the liver were: 1) loss of normal structure, hemorrhage and distortion of hepatic lobules; 2) cloudy swelling, degeneration, vacuolation and necrosis of liver cells; 3) infiltration of neutrophils. The lungs were injured and there were liver cell emboli in the small pulmonary arteries. Electron microscopy showed that the ultrastructure of the liver cells was severely damaged and the cells had significant features of necrosis. Conclusions: The major pathomorphological changes in the liver after impact injury are hemorrhage and necrosis. They may be complicated by exfoliation of liver cells to hepatic sinusoids. These cells circulate with the blood to form emboli in the pulmonary blood vessels.展开更多
基金Supported by the National Natural Science Foundation of China,No. 30230320National Science Fund for Distinguished Young Scholars from NSFC, No. 39925031National High Technology Research and Development Program of China, 863 grant 2004 AA215242Major State Basic Research Development Program of China, No. 2001CB510005partially by E-Institute of Shanghai Universities
文摘AIM： To investigate the role of CXCL16 in the pathogenesis of immunological liver injury and to explore the possible mechanism ofT lymphocyte infiltration regulated by CXCL16. METHODS： Immunological liver injury in murine model was induced by Bacille Calmette-Guerin and lipopolysaccharide. Expression pattern and distribution of CXCL16 were examined by real-time quantitative RT-PCR and immunohistochemical analysis. Anti-CXCL16 antibody was administrated in vivo to investigate its effect on T-cell recruitment and acute hepatic necrosis. The survival of murine model was also evaluated. RESULTS, The murine immunological liver injury model was successfully established, CXCL16 expression increased and predominantly distributed in periportal areas and vascular endothelia in injured liver tissues. Administration of anti-CXCL16 Ab protected the mice from death and acute liver damage. Approximately 70% of the mice survived for 72 h in the anti-CXCL16 Ab treatment group, whereas 80% died within 72 h in control Ab group. The number of liver-infiltrating T lymphocytes was significantly reduced from 1.01×10^7 to 3.52×10^6/liver, compared with control Ab treatment. CONCLUSION： CXCL16 is involved in immunological liver injury by regulating T lymphocyte infiltration in liver tissue.
文摘AIM： To evaluate the protective effects of preconditioning by α-lipoic acid （LA） in patients undergoing hepatic resection under inflow occlusion of the liver. METHODS： Twenty-four patients undergoing liver resection for various reasons either received 600 mg LA or NaCI 15 min before transection performed under inflow occlusion of the liver. Blood samples and liver wedge biopsy samples were obtained after opening of the abdomen immediately after inflow occlusion of the liver, and 30 min after the end of inflow occlusion of the liver. RESULTS： Serum levels of aspartate transferase and alanine transferase were reduced at all time points in patients who received LA in comparison to those who received NaCL. This was accompanied by reduced histomorphological features of oncosis. We observed TUNEL-positive hepatocytes in the livers of the untreated patients, especially after 30 min of ischemia. LA attenuated this increase of TUNEL-positive hepatocytes. Under preconditioning with LA, ATP content was significantly enhanced after 30 min of ischemia and after 30 min of reperfusion. CONCLUSION： This is the first report on the potential for LA reducing ischemia/reperfusion injury （IRI） of the liver in humans who were undergoing liver surgery. Beside its simple and rapid application, side effects did not occur. LA might therefore represent a new strategy against hepatic IRI in humans.
文摘Objective: To investigate the histopathological changes in the liver and other organs after impact injury. Methods: The rabbits were impacted with a BIM IV biological impacting machine at the xiphoid process. The severity of liver injury was graded and scored through gross anatomy. At the same time, the pathological changes in the liver, heart, and lung were observed by light and electron microscopes. Results: Light microscopy showed that the pathological changes in the liver were: 1) loss of normal structure, hemorrhage and distortion of hepatic lobules; 2) cloudy swelling, degeneration, vacuolation and necrosis of liver cells; 3) infiltration of neutrophils. The lungs were injured and there were liver cell emboli in the small pulmonary arteries. Electron microscopy showed that the ultrastructure of the liver cells was severely damaged and the cells had significant features of necrosis. Conclusions: The major pathomorphological changes in the liver after impact injury are hemorrhage and necrosis. They may be complicated by exfoliation of liver cells to hepatic sinusoids. These cells circulate with the blood to form emboli in the pulmonary blood vessels.
