ABSTRACT
Objective To investigate lipopolysaccharide (LPS) tolerance and its possible mechanism in experimental acute pancreatitis(AP) mice. Methods Two hundreds and ten C56BL/6J mice were randomized into normal saline(NS)+LPS group( n =105)and AP +LPS group( n =105). Both groups were subdivided into seven groups according to different dose of LPS. AP model was induced by intra- abdominal administration of cerulein (50 ?g/kg) for seven times at 1 hour interval. LPS was given 6 hours after first cerulein injection . Cerulein was replaced by NS in NS+LPS group. Ten mice in each sub- group were randomly selected to investigate mortality rate for 7 days. Another 5 mice were killed at 12 hours after the first cerulein injection. Liver, lung, kidney, pancreas and serum were reserved to evaluate pathological changes and measurement of amylase (AMS) and lactate dehydrogenase (LDH) levels. Gene expression profiles of leucocyte in NS+LPS(15 mg/kg)subgroup and AP+LPS(15 mg/kg)subgroup were studied with oligonucleotide microarrays of 12 479 full length mouse genes respectively for three times to screen the different genes between two groups. Results Mortality rates in both groups were increased, and correlated with the dosage of LPS. Mortality rate in AP+LPS group was significantly lower than that in NS+LPS group with the same LPS dose( P