CAJ | 학술논문

目的探讨大鼠急性出血坏死性胰腺炎(AHNP)并发胰性脑组织损害机理及评价纳屈酮治疗效果。方法应用5%牛磺胆酸钠逆行胰胆管注射诱发大鼠AHNP并发脑组织损害模型。实验分为对照组、胰性脑组织损害组(pancreatic encephalopathy, PE)及纳屈酮(NTX)治疗组，分别于6、12、24小时检测血浆及脑组织脂质过氧化产物丙二醛(MDA)含量、磷脂酶A2(PLA2)活性、氧自由基清除剂超氧化物歧化酶(SOD)活性、脑系数及胰腺和脑组织病理学改变。结果与对照组比较，PE组6、12、24小时血浆及脑组织中MDA含量及PLA2活性升高，SOD活性下降；光镜下见PE组6、12及24小时胰腺红细胞渗出、炎性细胞浸润及灶性坏死、脑组织水肿、点状出血和脱髓鞘改变； 6小时电镜下见胰腺细胞线粒体肿胀，嵴模糊，粗面内质网扩张； 12小时线粒体破损，粗面内质网脱颗粒； 24小时线粒体及粗面内质网破裂，次级溶酶体出现。NTX治疗组各时相血浆及脑组织MDA含量及PLA2活性较PE组低，SOD活性却较PE组高；且胰腺及脑组织的损害程度减轻。结论大鼠AHNP模型可引发胰性脑组织损害； NTX可降低血浆及脑组织氧自由基(OFR)含量、PLA2活性，同时增加SOD活性，进而减轻脑组织损害；延长大鼠生存时间及降低其病死率。
목적탐토대서급성출혈배사성이선염(AHNP)병발이성뇌조직손해궤리급평개납굴동치료효과。방법응용5%우광담산납역행이담관주사유발대서AHNP병발뇌조직손해모형。실험분위대조조、이성뇌조직손해조(pancreatic encephalopathy, PE)급납굴동(NTX)치료조，분별우6、12、24소시검측혈장급뇌조직지질과양화산물병이철(MDA)함량、린지매A2(PLA2)활성、양자유기청제제초양화물기화매(SOD)활성、뇌계수급이선화뇌조직병이학개변。결과여대조조비교，PE조6、12、24소시혈장급뇌조직중MDA함량급PLA2활성승고，SOD활성하강；광경하견PE조6、12급24소시이선홍세포삼출、염성세포침윤급조성배사、뇌조직수종、점상출혈화탈수초개변； 6소시전경하견이선세포선립체종창，척모호，조면내질망확장； 12소시선립체파손，조면내질망탈과립； 24소시선립체급조면내질망파렬，차급용매체출현。NTX치료조각시상혈장급뇌조직MDA함량급PLA2활성교PE조저，SOD활성각교PE조고；차이선급뇌조직적손해정도감경。결론대서AHNP모형가인발이성뇌조직손해； NTX가강저혈장급뇌조직양자유기(OFR)함량、PLA2활성，동시증가SOD활성，진이감경뇌조직손해；연장대서생존시간급강저기병사솔。
Objective　 To study the relationship between oxygen free radical and phospholipase A2 and therapeutic effect of naltrexone (NTX) on experimental pancreatic encephalopathy (PE) induced by acute hemorrhagic necrotizing pancreatitis (AHNP) in rats. Methods　 A model of experimental PE in AHNP was induced by retrograde injection of 5% sodium taurocholate into the pancreatic duct. The rats were randomly divided into three groups: control group, PE group and NTX group. The plasma and cerebral levels of malondialdenhyde(MDA), scavengers superoxided ismutase(SOD), and phospholipase A2 (PLA2) were determined in both PE and NTX groups. Changes of the pancreatic and cerebral histology were examined by light and electric microscopy. Results　In NTX treatment phase, the MDA and PLA2 were significantly fall, while SOD was increased in the plasma and cerebral tissue, the damage to pancreatic and cerebral tissue was emiliorated. Conclusion　The experimental model of PE on rats is an ideal one for PE investigation. NTX could decrease oxygen free radicals and PLA2 activity and improve the damage to cerebral and pancreatic tissue. The lethality rate in rats of PE is significantly low after NTX treatment.