| Hyperlipidemic pancreatitis, which is also called highblood triglycerides pancreatitis clinically, is the third cause ofillness, accounting for about1.3%to3.8%, only second to biliarypancreatitis and alcoholic pancreatitis and the morbidity is on therise with the improvement of people’s living standard as well asthe changing dietary structure of them. However, there is noconsensus on the pathogeny of the hyperlipidemic pancreatitis andmost researches focus on the toxic effect of non-esterified fattyacid, the entrainment of calcium overload and the gene mutation aswell. Therefore, with some newly-put arguments, what this paperaims is to have a further study on the entrainment of calciumoverload.Objective: This paper is intended to explore the role ofcalcium overload in the pathogeny of hyperlipidemic pancreatitisby observation of its curative effect after the application ofCalcium channel blockers verapamil to hyperlipidemic pancreatitisrats, which may lay a theoretical foundation for verapamil as a newdrug for hyperlipidemic pancreatitis.Methods:80SD male rats, eachat weight of200-250g, are grouped randomly into four, each group20. Sham Operation Group (SO): Ordinary emulsion feed (Ordinaryfeed+appropriate distilled water) Gavage administration on the rats for two weeks and laparotomy after that, stab pancreaticbiliary by empty needle, then withdraw the needle and close abdomen,no material injected. Severe Acute Pancreatitis Group (SAP):Ordinary emulsion feed fed rats two weeks after laparotomyretrograde cholangiopancreatography slow bolus injection of5%sodium taurocholate, the abdomen was closed. HyperlipidemicPancreatitis Group (HLP): High-fat fed agent (20%lard+10%cho-lesterol+20%Tween80+2%sodium cholate+1%propylthiouracil+amount of distilled water) for two weeks after administration,pancreatic duct puncture and injection5%sodium taurocholate, theabdomen was closed. Verapamil Treatment Group (CCB): Hyperlipidem-ic pancreatitis after modeling for10minutes, intraperitoneallyinjected verapamil1mg/kg. The number of the dead is totaled24hours after surgery and put all the rats to death, the amount ofascites recorded and blood triglyceride levels detected. Serumthromboxane A2(TXA2) by enzyme-linked immunosorbent assay (ELISA)and platelet-activating factor (PAF) content; Take the right amountof pancreatic tissue stained with hematoxylin-eosin (HE staining),pancreas under a microscope to observe the pathological changes ofpancreatic tissue injury and pathology score. Lastly, pancreatictissue with the proper amount of flow cytometry to detectintracellular calcium levels; analyze the expression of NF-κBp65 protein by Western blotting.Results:1. There are no rats died inSO group,7died in HLP group,4died in SAP group and2died inCCB group.2. There’s large amount of bloody ascites in SAP group,HLP group and CCB group, no ascites in SO group; TG levels in HLPand CCB group were significantly higher than those in the SO andSAP group, with statistical differences (P＜0.05).3. Pancreatictissue injury score: the extent of inflammation, edema, hemorrhage,necrosis in HLP and SAP group was significantly higher than thosein SO group (P＜0.05) and the level of injury in HLP was higher thanSAP group(P＜0.05), while inflammatory edema and hemorrhagicnecrosis in CCB group was significantly lower than the level of HLPGroup (P＜0.05).4. TXA2, PAF levels in HLP and SAP group weresignificantly higher than those in the control group (P <0.05) andHLP group was higher than the SAP group (P <0.05), while the CCBgroup TXA2, PAF levels were lower than the HLP group, which is ofstatistical significance (P <0.05).5. Calcium levels: HLP groupand SAP group was significantly higher than the SO group (P <0.05),calcium ions of HLP group is higher than SAP group, the differencebeing statistically significant (P <0.05), while the CCB group wassignificantly lower than HLP group (P <0.05).6. NF-κBp65proteinexpression: NF-κBp65strength and positive protein expressionwere significantly increased in HLP and SAP group (P <0.05) than the control group. There is significant difference in terms ofNF-κBp65HLP expression of strength and positive rate among HLP,SAP and CCB group (P <0.05).Conclusion:1.Rat model ofhyperlipidemia hyperlipidemia can be successfully established byfeeding with high fat emulsion modification （20%lard+10%cholesterol+20%Tween80+2%sodium cholate+1%propylene unit(PTU)+amount of distilled water）for two weeks. Retrogradecholangiopancreatography bolus injection of5%sodium taurocholatecan also result in severe acute pancreatitis.2.Hyperlipidemicpancreatitis is more serious than the common type of the diseasepancreatitis in rats，indicating that high cholesterol plays animportant role in promoting the occurrence and development ofpancreatitis.3. Hyperlipidemic pancreatitis in rats become lessserious through the use of calcium channel blockers inhibit thecalcium overload in pancreatic acinar cell, which signifies thatcalcium overload involved the disease process of hyperlipidemicpancreatitis and that verapamil takes effect in the treatment ofhyperlipidemic pancreatitis. |
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