CAJ | 학술논문

目的:探讨重症急性胰腺炎对胰腺细胞线粒体和溶酶体脂质过氧化损伤及栀子的保护作用.方法:将SD大鼠经胰管逆行注射1.5%去氧胆酸钠建立重症急性胰腺炎模型,随机分为对照组、模型组和栀子治疗组,观察胰腺细胞线粒体、溶酶体超氧化物歧化酶(SOD)、丙二醛(MDA)、膜流动性以及胰腺细胞线粒体琥珀酸脱氢酶(SDH)活性、溶酶体酸性磷酸酶(ACP)释放率及栀子对上述指标的影响.结果:与对照组比较,模型组胰腺线粒体、溶酶体SOD活性、膜流动性明显降低,MDA含量增高,线粒体SDH活性下降,而溶酶体ACP释放率增加(P ＜ 0.01);栀子治疗后上述各检测指标均较模型组明显改善(P ＜ 0.01);相关分析显示MDA与SOD间存在明显负相关,MDA与膜流动性间呈显著正相关(P ＜ 0.01).结论:栀子通过清除重症急性胰腺炎时胰腺亚细胞器氧自由基,对抗脂质过氧化,保护胰腺亚细胞器结构和功能的正常.
목적:탐토중증급성이선염대이선세포선립체화용매체지질과양화손상급치자적보호작용.방법:장SD대서경이관역행주사1.5%거양담산납건립중증급성이선염모형,수궤분위대조조、모형조화치자치료조,관찰이선세포선립체、용매체초양화물기화매(SOD)、병이철(MDA)、막류동성이급이선세포선립체호박산탈경매(SDH)활성、용매체산성린산매(ACP)석방솔급치자대상술지표적영향.결과:여대조조비교,모형조이선선립체、용매체SOD활성、막류동성명현강저,MDA함량증고,선립체SDH활성하강,이용매체ACP석방솔증가(P ＜ 0.01);치자치료후상술각검측지표균교모형조명현개선(P ＜ 0.01);상관분석현시MDA여SOD간존재명현부상관,MDA여막류동성간정현저정상관(P ＜ 0.01).결론:치자통과청제중증급성이선염시이선아세포기양자유기,대항지질과양화,보호이선아세포기결구화공능적정상.
Objective: To explore lipid peroxidation injuries of pancreatic mitochondria and lysosome following severe acute pancreatitis (SAP) and the protective effects of gardenia jasminoides ellis (GJE) thereof. Methods: SAP models were induced by retrograde injection of 1.5% sodium deoxycholate. The rats were randomly divided into three groups: sham group, SAP group and GJE group. The changes were measured in superoxide dismutase (SOD), malondialdehyde (MDA), membrane fluidity of mitochondria and lysosome in pancreas and succinic dehydrogenase (SDH) in mitochondria, acid phosphatase (ACP) in lysosome.The effects of GJE were also observed. Results: Compared with Sham group, the activity of SOD and membrane fluidity of mitochondria and lysosome were decreased in pancreas, and the content of MDA were increased; the releasing rate of ACP was significantly higher in lysosome; SDH in mitochondria was lower in SAP group(P < 0.01). The above-mentioned indexes were obviously ameliorated in GJE group than those in SAP group(P < 0.01). The correlation analysis indicated that MDA was negatively correlated with SOD, positively correlated with membrane fluidity (P < 0.01). Conclusion: GJE can alleviate lipid peroxidation by getting rid of oxygen free radicals of pancreatic subcellular fraction in the course of SAP, and protect the structure and function of pancreatic subcellular fraction.