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机构地区:[1]义乌市中心医院普通外一科,浙江金华322000 [2]广东医学院附属医院肿瘤中心,广东湛江523808 [3]青海大学附属医院肝胆胰外科,青海西宁810001
出 处:《温州医科大学学报》2016年第5期344-347,共4页Journal of Wenzhou Medical University
基 金:国家自然科学基金青年科学基金资助项目(81201672);义乌市人才引进立项项目(2012-R-04)
摘 要:目的:H_2S对肠缺血-再灌注损伤大鼠凝血功能异常的影响及机制。方法:24只雄性Wistar大鼠随机分为A(假手术)组、B(缺血-再灌注)组和C(缺血-再灌注+NaHS)组。建立大鼠肠缺血-再灌注损伤模型,再灌注前10 min C组大鼠经尾静脉注入100μmol/kg NaHS并以1 mg/(kg·h)速度静脉维持到再灌注2h。RT-PCR、流式细胞仪法分别检测单核细胞蛋白酶激活受体-1(PAR-1)、PAR-3 m RNA及蛋白表达;ELISA法检测血组织因子(TF)、TNF-α、组织型纤溶酶原激活物(t-PA)、纤溶酶原激活物抑制剂-1(PAI-1);敏感硫电极法测定血H2S;检测凝血VIII因子活性(FVIII:C)、血管性血友病因子(v WF)、纤溶酶原活性(PLG:A)、抗凝血酶活性(AT:A)、血小板计数。结果:C组PAR-1、PAR-1 m RNA、TF、TNF-α、FVIII:C、v WF、t-PA、PAI-1均低于B组、高于A组,差异有统计学意义(均P<0.01);C组H2S、PLG:A、AT:A低于A组、高于B组,差异有统计学意义(均P<0.01)。H_2S与PAR-1、PAR-1 m RNA、TF、TNF-α、FVIII:C、v WF、t-PA、PAI-1呈负相关(r=-0.58、-0.68、-0.62、-0.64、-0.73、-0.55、-0.57、-0.64,均P<0.01),与PLG:A、AT:A呈正相关(r=0.57、0.61,均P<0.01)。结论:H_2S通过降低PAR-1、TF、TNF-α含量,改善大鼠肠缺血-再灌注损伤时的凝血功能异常。Objective: To study the effects of hydrogen sulfide on coagulation dysfunction in rats with in-testinal ischemia-reperfusion injury and its mechanism. Methods: Twenty-four male Wistar rats were randomly divided into three groups (8 in each group): sham operation group (group A), ischemia-reperfusion group (group B), ischemia-reperfusion and sodium hydrosulfide group (group C). The animal model of intestinal ischemia-re- perfusion was established. Rats in Group C were received sodium hydrosulfide (100 I.tmol/kg bolus+l rag- kg-l. h-1 infusion) 10 min prior to the onset of reperfusion. Expressions of PAR-1 and PAR-3 were detected by RT-PCR and flow cytometry. Serum H2S was tested by sensitive sulfide electrode. Serum TF, TNF-α, t-PA, PAI-1 were determined by ELISA. PLG:A, FVIII:C, vWF, AT:A, platelet were measured. Results: PAR-I, PAR-1 mRNA, TF, TNF-α, FVIII:C, vWF, t-PA, PAl-1 in group C were significantly higher than those in group A, predominantly lower than those in group B (P〈0.01). H2S, PLG:A, AT:A in group C were sharply higher than those in group B, strikingly lower than those in group A (P〈0.01). H2S negatively correlated with PAR-l, PAR-1 mRNA, TF, TNF-α, FVIII:C, vWF, t-PA, PAI-1 (r=-0.58, -0.68, -0.62, -0.64, -0.73, -0.55, -0.57, -0.64, P〈0.01), posi- tively correlating with PLG:A, AT:A (r=0.57, 0.61, P〈0.01 ). Conclusion: H2S attenuates coagulation dysfunction in rats with intestinal ischemia-reperfusion injury by down-regulating PAR-l, TF, TNF-cc
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