机构地区: 南京农业大学动物医学院
出 处: 《畜牧兽医学报》 1998年第4期371-376,共6页
摘 要: 本文探讨内毒素诱导肺脂质过氧化损伤机制及山莨菪碱(654-2)对其保护作用。将36头杂交山羊随机分成3组。第Ⅰ组作为对照,第Ⅱ组和第Ⅲ组静注大肠杆菌内毒素两次,间隔24h,第Ⅲ组于第二次注射内毒素前10min静注654-2,各组于5h、12h剖杀6头,检测肺组织抗氧化系统功能。结果表明:第Ⅱ、Ⅲ组肺组织MDA含量明显增加(P<0.01),Ⅲ组显著低于Ⅱ组(P<0.01),GSH-Px、总SOD、Mn-SOD、CuZn-SOD活性明显降低(P<0.01,P<0.05),除12hGSH-Px活性Ⅱ与Ⅲ组差异不显著(P>0.05)外,第Ⅲ组各种酶活性显著高于Ⅱ组(P<0.01,P<0.05);肺组织GSH、T-SH、NP-SH和PB-SH含量亦明显下降(P<0.05),且Ⅱ组低于Ⅲ组(P<0.01,P<0.05)。提示内毒素能明显导致肺组织脂质过氧化作用,而提前给予654-2能显著减轻氧自由基对肺的损伤。 おung lipid peroxidation injury induced by endotoxin and the preventive mechanism of anisodamine(654—2)were studied in the paperThirty six hybrid goats were randomly divided into three groupsGroup I was the normal controlThe goats of group Ⅱand Ⅲwere intravenously injected EColi endotoxin and group Ⅲ were intravenously injected anisodamine (25mg/kg)for 10 minutes before endotioxin injectionThe lung antioxidant functions were examined at 5h and 12h postinjectionThe results showed that the antioxdant functions of lung tissue were significantly decreased in group Ⅱand ⅢLung tissues MDA contents significantly increased in group Ⅱ and Ⅲ,but lung MDA contents of group Ⅲ were significantly lower than those of group ⅢThe activities of GSH—Px and total SOD,CuZn—SOD and Mn—SOD in group Ⅱ and Ⅲ significantly reduced (P<001,P<005)The activities of lung GSH—Px and totoal SOD,CuZn—SOD antivities at 5h and 12h of group Ⅲ were significantly higher than those of group ⅢThe contents of lung tissues GSH,total sulfhydryl group,protein—bound and nonprotein bound sulfhydryl group of group Ⅱ and Ⅲ decreased at 5h and 12hThe experimental antioxidant parameters indicated that endotoxin could significantly induce lung lipid peroxidation injury and anisodamine added for 10 minutes bofore endotoxin administration could significantly attenunate lung injury induced by oxygen free radicals