摘要
AIM： To investigate the influence of neutrophil adhesion molecule blockade with rnonoclonal antibody （MoAb CD11b） and E. coli lipopolysaccharide （LPS） administration on experimental acute pancreatitis （AP）. METHODS： AP was induced by four ip injections of cerulein （Cn） at 1-h intervals. MoAb CD 11b and LPS were administered at the beginning of the experiment. RESULTS： The neutrophil count and chemiluminescence were diminished at the beginning of AP. The oxidative stress parameters were found within the pancreatic gland. MoAb CD 11b used for AP resulted in a significant reduction of pancreatic infiltration and pancreatitis oxidative stress parameters. Serum interleukin-6 （IL-6） was not detected in AP animals, whereas high serum IL-6 concentration was noted only in animals receiving LPS. CONCLUSION： Neutrophils are involved in pancreatic damage in the early stage of AP. Neutrophil infiltration reduction protects the pancreatic gland from destruction during AP. LPS does not change the early course of Cn pancreatitis in rats.
AIM: To investigate the influence of neutrophil adhesion molecule blockade with monoclonal antibody (MoAb CD11b) and E. coli lipopolysaccharide (LPS)administration on experimental acute pancreatitis (AP).METHODS: AP was induced by four ip injections of cerulein (Cn) at 1-h intervals. MoAb CD 11b and LPS were administered at the beginning of the experiment.RESULTS: The neutrophil count and chemiluminescence were diminished at the beginning of AP. The oxidative stress parameters were found within the pancreatic gland. MoAb CD 11b used for AP resulted in a significant reduction of pancreatic infiltration and pancreatitis oxidative stress parameters. Serum interleukin-6 (IL-6)was not detected in AP animals, whereas high serum IL-6 concentration was noted only in animals receiving LPS.CONCLUSION: Neutrophils are involved in pancreatic damage in the early stage of AP. Neutrophil infiltration reduction protects the pancreatic gland from destruction during AP. LPS does not change the early course of Cn pancreatitis in rats.
基金
Supported by the grant from Medical University of Gdansk,Poland
