| I. The induction of the rat model of the severe acute pancreatitisassociated with cerebral damageObjective: To induce the model of the brain damage in severe acute pancreatitis (SAP)in rats. To provide rat models for the second and the third parts of this study. Methods:Sixty male Sprague-Dawley rats were randomly divided into six groups: normal controlgroup 3,6,12 hour and SAP group 3,6,12 hour. Each group included 10 rats. SAP modelwas established by retrograde injection of 5% sodium taurocholate into pancreatic duct. Aseries of blood, pancreatic tissue and brain tissue samples were obtained at 3,6 and 12hours after operation respectively. Hemodiastase, water content and the count of leucocytesaccumulation and adhesion of the brain tissue were measured. Histopathological change ofpancreas and brain were observed. Results: Compared with normal control group,levels ofhemodiastase,histopathological score of the rat pancreas,the count of leucocytesaccumulation and adhesion of the brain tissue significantly increased at each time point inSAP group (P﹤0.01) and levels of water content of the brain tissue,histopathologicalscore of the rat brain increased at 6 and 12 hours in SAP group(P﹤0.01～0.05). All ofthem were gradually increased at 3,6 and 12 hours in SAP group(P<0.01 or 0.05).Histopathological score of the rat brain were correlated with histopathological score of therat pancreas at 6 and 12 hours in SAP group(r=0.72,P<0.01). Conclusions: The model ofthe brain damage in SAP can be established by retrograde injection of 5% sodiumtaurocholate into pancreatic duct. It can be duplicated and reproduced easily. II. The role of mediators of inflammation on cerebral damage caused bysevere acute pancreatitis in ratsObjective: To study the role of mediators of inflammation on cerebral damage causedby severe acute pancreatitis in rats. Methods: Sixty male Sprague-Dawley rats wererandomly divided into six groups: normal control group 3,6,12 hour and SAP group 3,6,12 hour. Each group included 10 rats. SAP model was established by retrogradeinjection of 5% sodium taurocholate into pancreatic duct. A series of blood and brain tissuesamples were obtained at 3,6 and 12 hours after operation respectively. Levels of MDA inthe brain tissue, TNF-a in the blood and brain tissue were measured with ELISA. Levels ofNF-κB p65 mRNA in the rat brain tissue were measured by RT-PCR. Results:Comparedwith normal control group,levels of MDA,TNF-a and NF-κB p65 mRNA in the braintissue,levels of TNF-a in the blood significantly increased at each time point in SAPgroup(P<0.01 or 0.05). All of them were gradually increased at 3,6 and 12 hours in SAPgroup(P<0.01 or 0.05). Levels of MDA,TNF-a and NF-κB p65 mRNA in the brain tissueand histopathological score of the rat brain were correlated with each other at 6 and 12hours in SAP group(r=0.77,0.82,0.78,0.84,0.82,0.70,P<0.01). Conclusions: It is clearthat free radical,NF-κB p65 and TNF-a can play an important role on cerebral damagecaused by SAP in rats.III. The protective effects of edaravone on cerebral damage caused bysevere acute pancreatitis in ratsObjective:To study the protective effects of edaravone on cerebral damage caused bysevere acute pancreatitis(SAP) in rats. Methods:A total of 60 male Sprague-Dawley ratswere randomly divided into SAP group 3, 12 hour, treated group 3, 12 hour and positivecontrol group 3, 12 hour. Each group included 10 rats. A series of blood,pancreatic tissueand brain tissue samples were obtained at 3 and 12 hours after operation respectively.Hemodiastase,histopathological change of pancreas and brain were observed. The levels of TNF-a in the blood and brain tissue were measured with ELISA.Water content,MDA,the count of leucocytes accumulation and adhesion of the brain tissue were measured.Levels of NF-κB p65 mRNA in the rat brain tissue were measured by RT-PCR. Results:Compared with SAP group 12 hour,levels of hemodiastase,histopathological score of therat pancreas,the count of leucocytes accumulation and adhesion of the brain tissue,watercontent of the brain tissue,histopathological score of the rat brain,TNF-a in the blood andbrain tissue,MDA and NF-κB p65 mRNA in the brain tissue significantly decreased at 12hours in treated group and positive control group(P<0.01 or 0.05). However,there were noobvious difference in all indexes at 12 hours between the treated group and positive controlgroup (P﹥0.05). Conclusion:It is possible that edaravone can clean up free radical,inhibit NF-κB activities,reduce TNF-a or other cytokines in rat brain and inhibitinflammatory response,and play a protective role on cerebral damage caused by SAP inrats.
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