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机构地区:[1]福建医科大学省立临床学院福建省立医院消化内科,福建省福州市350001
出 处:《世界华人消化杂志》2009年第25期2561-2565,共5页World Chinese Journal of Digestology
摘 要:目的:观察高脂血症对大鼠急性胰腺炎病情的影响,探讨脂质过氧化损伤在伴高脂血症重症急性胰腺炎(SAP)中的作用及其机制.方法:SD大鼠脂肪乳剂灌胃2wk建立高脂血症模型,逆行胰胆管注射3.5%牛磺胆酸钠诱发SAP模型.将大鼠50只随机分为4组:正常组(n=10);高脂血症对照组(HL组,n=10);SAP组(n=15);伴高脂血症SAP(HAP,n=15).检测血清淀粉酶(AMS)、甘油三酯(TG)及胆固醇(CH)水平,并检测血清及胰腺组织的丙二醛(MDA)、超氧化物歧化酶(SOD)、黄嘌呤氧化酶(XOD)、一氧化氮(NO),观察胰腺组织病理改变.结果:HAP组胰腺组织病理改变较SAP组严重;HAP组血清及胰腺组织MDA、XOD水平显著高于SAP组(血清:30.76±2.67nmol/mLvs23.14±3.42nmol/mL,55.72±10.49U/Lvs45.78±8.98U/L,均P<0.01;胰腺组织:4.33±0.48nmol/mgprotvs2.87±0.45nmol/mgprot,5.57±0.63U/gprotvs4.33±0.79U/gprot,均P<0.01);其血清及胰腺组织SOD、NO水平显著低于SAP组(血清:85.46±13.56U/mLvs97.16±13.77U/mL,31.72±10.50μmol/Lvs52.97±6.01μmol/L,均P<0.05;胰腺组织:22.65±3.85U/mgprotvs27.88±4.43U/mgprot,均P<0.01;1.09±0.21μmol/gprotvs1.48±0.40μmol/gprot,均P<0.05).结论:高脂血症可加SAP的胰腺病理改变;脂质过氧化损伤可能在高脂血症加重SAP的机制中发挥重要作用.AIM: To investigate the role of lipid peroxidation in the development of severe acute pancreafifis (SAP) in rats with hyperlipemia (HP).METHODS: Sprague-Dawley (SD) rats were administered intragastrically a high-fat diet for two weeks to induce experimental HP. SAP was induced by retrograde injection of 3.5% sodium taurocholate into the pancreatic duct. Fifty male Sprague-Dawley rats were randomly divided into four groups: normal control group, HL group, SAP group and HAP (HL+SAP) group. The levels of amylase (AMS), triglyceride (TG) and cholesterol (CH) in the serum were mea- sured. The changes in the concentrations of malonaldehyde (MDA), superoxide dismutase (SOD), xanthine oxidase (XOD) and nitric oxide (NO) in the serum and pancreatic tissue were RESULTS: The pathological changes in the pan- creas were more severe in the HAP group than in the SAP group. The levels of MDA and XOD in the serum and pancreatic tissue were signifi- cantly higher in the HAP group than in the SAP group (serum: 30.76 + 2.67 nmol/mL vs 23.14 + 3.42 nmol/mL and 55.72 + 10.49 U/L vs 45.78 + 8.98 U/L, both P 〈 0.01; pancreatic tissue: 4.33 + 0.48 nmol/mgprot vs 2.87 + 0.45 nmol/mgprot and 5.57 + 0.63 U/gprot vs 4.33 + 0.79 U/gprot, both P 〈 0.01), while the levels of SOD and NO in the serum and pancreatic tissue were signifi- cantly lower in the HAP group than in the SAP group (serum: 85.46 + 13.56 U/mL vs 97.16 + 13.77 U/mL and 31.72 + 10.50 ~mol/L vs 52.97 + 6.01 ganol/L, both P 〈 0.05; pancreatic tissue: 22.65 + 3.85 U/mgprot vs 27.88 + 4.43 U/mgprot and 1.09 + 0.21 ~mol/gprot vs 1.48 + 0.40 ~mol/ gprot, both P 〈 0.05).CONCLUSION: Hyperlipemia can aggravate pancreatic pathological changes caused by se- vere acute pancreatitis in rats perhaps through induction of lipid peroxidation.
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