| IntroductionAcute necrotizing pancreatitis (ANP) is a common disease that seriously threats human health. Now people realize that once the disease episode, it will worsen gradually and lead to multiple system organ failure ( MSOF) which may cause patient to die. Thouth we treat it with inhibitor of pancreatin and 玽en with surgical operation to clean pancreatic necrosis tissue, it can not prevent disease from continual deterioration. Previous view and program on treatment focus on pancreatic autodigestion which make treatment in passive situation. Since acute pancreatitis' theory of leucocyte overactivation was proposed by Rindernecht from 1988, the important role of immunological mechanisms was widely accepted. So, inhibiting overreaction of immune in ANP may be the most hopeful method.Complement is an important part of humoral immunity. Its principal physiology function is to facilitate swollowing and lysising target. cell and may play important role on cleaning foreign microorganism and antigen. On the other hand, inflammatory reaction caused by ana-phylatoxin which is generated through complement overactivation may cause injury to normal tissue and cell. Complement protein attracts many foreign researchers' attention because of its quality of intense inflammation and so does membrane attact complex ( MAC) for itspowerful destructiveness. Many researchers confirm that activation of complement system plays an important role during the development of AP and takes part in the processes of inflammatory reaction. So how to inhibit complement from activating and interrupt amplification of cascade reaction may be direction of treatment of AP.Being cascade reaction, complement activation is strictly controlled by many regulators of complement activation. Among these regulators, membrane cofactor protein ( MCP),decay acceleration factor (DAF), membrane inhibitor of reactive lysis ( CD59,MIRL) are more effective. Connected with cell surface, these three regulators inhibit complement activation through suppressing variously key enzyme in the activation of complement and as a result, relieve inflammation reaction. Recently, many scientists have done lots of research about these three protein, they found these proteins play key roles in sep-temia,ischemical reperfusion injury of myocardium and intestines , a-cute respiratory distress syndrome and transplantation rejection. But no report has been shown about RCA during ANP. We set about investigating effects of RCA in ANP. Our research aims to explain effects of RCA during ANP through observation of MCP,DAF,CD59 in ANP.Materials1. main drugs and reagents : sodium taurocholate ( sigma, America) , MCP (sc - 7056 ),DAF ( sc - 9156 ),CD59 ( sc - 9157 ) poly-clonal antibody ( Santa Cruz ) , SABC immunohistochemistry kit (Boster, Wuhan).2. Main device and equipments: centrifuge ( SIMENS , German ) N cryogenic refrigerator ( MDF - U40856 ), frozen microtome (BRIGHT1512, England).3. Experimental animals: Wistar rat ( n = 50 ) , supplied by animal lab of CMU.Methods1. Animals and groups : Fifty Wistar rats of both sexes , weighting 180 to 200g , were divided into five groups (n = 10) randomly, one group of control and four groups of ANP ( represent 3,6,12,24h of AP respectively).2. Induction of ANP : ANP model was established by retrograde injection method. All animals were anesthetized with an intraperitone-al injection of 2% sodium pentobarbital (0.1ml/100g weight). After entering abdominal cavity, we exposed pancreas and then retrogradely punctured biliopancreatic duct at papilla of duodenum. A artery clamp was placed on the bile duct to the liver. 1 ml/Kg of 5% sodium tauro-cholate were injected into the common biliopancreatic duct under steady manual pressure at a speed of 0. 2ml/min. After injection, we blocked up the puncture site for 5 min in order that drug would not spil over . Animals in control group were treated only by turning over of pancreas.3. Disposal and collection of specimen ; Animal...
|
PDF Full Text Request