| Objective To build a rat model with hyperlipidemia and acute necrotizing pancreatitis(HAP), observing the expression of migration inhibitory factor (MIF) and tumor necrosisfactor-α(TNF-α)in blood and pancreas, exploring the possible effect of MIF in thepathogenesis of HAP.Methods Fifty healthy male SD rats were randomly divided into two groups: basic feedgroup (N=20) and high fat feed group (N=30), respectively feeding basic diet andhigh-fat diet(which consist of87.8％nomal diet,10%lard,2%cholesterol and0.2%sodium cholate) for4weeks. Then the basic diet group was randomly divided intotwo groups: Control group (group C, N=5) and ANP group (N=15). The high-fat dietgroup was randomly divided into two groups: HL group (N=15) and HAP group (N=15).Group C and HL group were induced by retrograde injection of NS. ANP group and HAPgroup were induced by retrograde injection of3.5%sodium taurocholate into thebiliopancreatic duct. Rats were sacrificed at4h，9h，24h later respectively. Blood andpancreas tissues were gained. The level of serum MIF and TNF-αwas determined withELISA. Serum triglyceride (TG) and diastase(Amyl) was measured by fully automaticclinical biochemical analyzer. The expression of MIF in pancreatic tissue was observed bythe immunohistochemical staining. Pancreatic histopathology was observed by lightmicroscopy.Results (1) Serum TG of rats fed with high-fat diet was higher than that of rats fed withbasic diet (P<0.01); serum amylase and pancreatic histopathological score in both ANPgroup and HAP group was higher than that of group C (P<0.01).(2) Compared with groupC, serum MIF and TNF-αlevel in both ANP group and HAP group began to rise at4hafter the induction of AP, and remained high at both9h and24h (P<0.05).(3) Serum MIFlevel in HAP group had no significant difference from that in ANP group (P>0.05). SerumTNF-α level was higher in HAP group only at24h (P<0.01), but had no significantdifference in both4h and9h in HAP group (P>0.05), compared with that in ANP group.(4) Positive correlation was found between pancreatic histopathological score, serum MIF and TNF-αlevel in both ANP group and HAP group (P<0.05).(5) There was almost noexpression of MIF in pancreatic tissue in Group C.The average gray scale in both ANP24h group and HAP24h group was significantly higher than that in group C (P<0.05), butthe average gray scale of MIF in HAP group had no significant difference from that inANP group (P>0.05).Conclusions (1) A model of HAP complicated with hyperlipemia in rat can be developedby feeding high-fat diet for4weeks and retrograde injection of3.5%sodium taurocholateinto the biliopancreatic duct.(2) The expression of MIF increases early in HAP, indicatingthat MIF is involved in the occurrence and development of HAP.(3) Positive correlation isfound between serum MIF and TNF-α, suggesting that MIF may be involved in thepathogenesis of HAP, and the biological effect is correlated with the release of TNF-α.(4)Hyperlipidemia doesn’t participate in the expression of the MIF. |
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