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作 者:张素斌[1] 秦科[1,2] 黄国勇[1] 莫宁[1,3] 梁东科[1]
机构地区:[1]广西医科大学第一附属医院急诊科,南宁530021 [2]中国人民解放军第303医院器官移植中心,广州军区肝、肾移植中心 [3]广西医科大学药学院
出 处:《广西医科大学学报》2012年第3期349-352,共4页Journal of Guangxi Medical University
基 金:广西自然科学青年基金资助项目(No.桂科青0832027)
摘 要:目的:研究体外循环(CPB)后脑组织的一氧化氮合成酶(NOS)活性的变化及单唾液酸神经节苷脂(GM1)干预后对其的影响。方法:选用雄性SD大鼠,经右颈静脉插管引流,尾动脉插管灌注建立CPB(CBP组),转流时间l h,建立CPB动物模型。随机分为CPB模型组、CPB模型+GM1组、输血组和假手术组,每组10只。脑组织匀浆测定结构型一氧化氮合成酶(cNOS)、诱导型一氧化氮合成酶(iNOS)和NO活性。结果:CPB组脑组织中的iNOS活性由正常的(16.47±2.52)pmol/mg.prot-1.min-1增加到(69.84±8.73)pmol/mg.prot-1.min-1(P<0.01),CPB模型+GM1组则增加到(57.86±7.79)pmol/mg.prot-1.min-1(P<0.01),与CPB组比较差异有统计学意义(P<0.05);CPB组脑组织中的cNOS活性由正常的(57.74±8.78)pmol/mg.prot-1.min-1下降到(32.67±6.61)pmol/mg.prot-1.min-1(P<0.01),CPB模型+GM1组则下降到(42.72±7.23)pmol/mg.prot-1(P<0.05),与CPB组比较差异有统计学意义(P<0.05);CPB组脑组织中的NO含量由正常的(258.91±48.17)pmol/mg.prot-1增加到(713.74±98.43)pmol/mg.prot-1(P<0.01),CPB模型+GM1组则增加到(523.74±87.36)pmol/mg.prot-1(P<0.01),与CPB组比较差异有统计学意义(P<0.05)。结论:CPB脑损伤与iNOS产生大量的NO导致的神经毒性作用有关;GM1在一定程度降低了脑中活化的iNOS含量,减少了NO的分泌释放,具有一定的脑保护作用。Objective:To observe the effect of GM1 on nitric oxide synthase (NOS), including constitutive nitric oxide synthase (cNOS) and induced nitric oxide synthase (iNOS) following cerebral damage after CPB in rats. Methods: SPF-class adult male SD rats were randomly divided into CPB, CPB+GM1, trans- fusion, and sham-operated groups. After establishing a rat model of cardiopulmonary bypass, GM1 with 20 mg/kg was added to the priming solution. All rats were anesthetized to collect the whole cerebral tissues for detecting the activity of cNOS, iNOS and NO content after 24 hours. Results: Compared with the con- trol group, the level of iNOS and NO increased significantly ( P 〈0. 05), while the cNOS activity de- creased significantly ( P 〈0.05) in the CPB group. GM1 administration obviously descended the activity of iNOS and NO and increased the cNOS activity. Conclusion: The rise of iNOS activity could correlate close- ly with brain injury after CPB, and GM1 could reduce iNOS activity and NO content. GM1 has the effect of brain protection against the neurotoxicity of NO.
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