Intrapulmonary expression of intercellular adhesion molecule-I in\\r\\r\\r\\r\\r\\r\\r

• 作 者: 罗昆仑 何振平 李昆 段恒春 马宽生
• 出 处: Journal of Medical Colleges of PLA
• 发表日期: 1998年03期
• 关键词: intercellular weighing

intrapulmonary expression of intercellular adhesion molecule- I (ICAM-l ) in acute hemorrhagicnecrotic pancreatitis (AHNP) and its significance were studied with imrnunohistochemistry and computer image analysis system and the therapeutic efficacy of the monoclonal antibody of tumor necrosis factora (TNFaMnAb ) was evaluated in rats. It was found during AHNP, there was an early increase of intrapulmonary expression of ICAM--l and the expression reached the peak in the 12th hour after the onset of AHNP and became stabilized in the 24th hour. ICAM-l expression correlated positively to the accumulation of polymorphonuclear neutrophils (PMNs). ICAM-l expression and PMN accumulation would be significantly attenuated if the rats were pretreated with TNFa MnAb. It is concluded that PMN infiltration in the pulmonary tissues results from intrapulmonary expression of ICAM-l and TNFa MnAb inhibits ICAM-l expression andPMN accumulation in the lungs. Consequently, administration of TNFa MnAb during AHNP can protect thelungs from being damaged.

intrapulmonary expression of intercellular adhesion molecule-I (ICAM-1) in acute hemorrhagic necrotic pancreatitis (AHNP) and its significance were studied with imrnunohistochemistry and computer image analysis system and the therapeutic efficacy of the monoclonal antibody of tumor necrosis factora (TNFaMnAb) was as in rats. It was found during AHNP, there was an early increase of intrapulmonary expression of ICAM-1 and the expression reached the peak in the 12th hour after the onset of AHNP and became stabilized in the 24th hour. to the accumulation of polymorphonuclear neutrophils (PMNs). ICAM-1 expression and PMN accumulation would be significantly attenuated if the rats were pretreated with TNFa MnAb. It is said that that PMN infiltration in the pulmonary tissues results from intrapulmonary expression of ICAM-1 and TNFa MnAb inhibits ICAM-1 expression and PMN accumulation in the lungs. Consequently, administration of TNFa MnAb during AHNP can protect thelungs from being damaged.