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出 处:《时珍国医国药》2010年第8期1849-1851,共3页Lishizhen Medicine and Materia Medica Research
基 金:国家自然科学基金(No.30660228);广西教育厅科研项目(No.2004-20);广西中医学院高学历科研启动金资助
摘 要:目的在前期工作基础上,对灯盏乙素对脂多糖加卡介苗所致小鼠免疫性肝损伤保护作用的机制进行研究。方法建立脂多糖加卡介苗(LPS+BCG)致小鼠免疫性肝损伤模型,灯盏乙素50,100,200 mg.kg-1,1次/d,连续灌胃给药12d。测定血清中谷丙转氨酶(alanine aminotransferase,ALT)及肝组织匀浆中超氧化物歧化酶(superoxide dismutase,SOD)、丙二醛(malondialdehyde,MDA)、谷胱甘肽过氧化物酶(glutathione peroxidase,GSH-Px)、过氧化氢酶(catalase,CAT)、黄嘌呤氧化酶(xanthine oxidase,XOD)、一氧化氮(nitric oxide,NO)、总一氧化氮合酶(total Nitricoxide synthase,total NOS)、结构型一氧化氮合酶(Constitutive Nitricoxide synthase,cNOS)、诱导型一氧化氮合酶(Inducible Nitricoxide synthase,iNOS)等生化指标。结果灯盏乙素低、中、高3个剂量组均能显著降低LPS+BCG致肝损伤小鼠血清中ALT水平,各剂量组能不同程度提高肝组织匀浆中CAT,SOD,GSH-Px的活性以及降低XOD,MDA,NO的含量。对一氧化氮合酶各分型分析表明,灯盏乙素能显著降低总NOS和iNOS的表达,对cNOS的表达基本没有影响。结论灯盏乙素对脂多糖加卡介苗引起的免疫性肝损伤具有保护作用的机制可能与其抗脂质过氧化,增强机体对自由基的清除能力及调节体内NO水平等有关。Objective To investigate the mechanism of the protection of scutellarin against immunological liver injury induced by BCG+LPS in mice according to our previous study.MethodsExperimental immunological liver injury model was created by Calmette-Guerin bacillus vaccine(BCG) and lipopolysaccharide(LPS) in mice.Mice were treated with scutellarin 50,100,200 mg·kg-1 through oral gavage once daily for 12 consecutive days.The level of ALT in serum,the contents or activities of SOD,MDA,GSH-Px,CAT,XOD,NO,total NOS,iNOS,cNOS in liver tissues were monitored.Results Three doses of scutellarin(50,100,200 mg·kg-1) could significantly decrease the level of ALT,significantly increase the activities of CAT,SOD,GSH-Px,and decrease the contents of SOD,MDA,NO in liver tissue.According to NOS analysis,scutellarin could decrease the expression of total NOS and iNOS,but it had no effect on the expression of cNOS.ConclusionThe mechanism of the protection of scutellarin on immunological liver injury induced by BCG+LPS in mice might attribute to preventing lipid peroxidation,reinforcing capability of free radical clearance,adjusting the level of NO in the body.
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