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作 者:任倩倩[1] 韩冲芳[2,3] 李婧[1] 乔冠中[4]
机构地区:[1]山西医科大学研究生院,030001 [2]山西医学科学院 [3]山西大医院麻醉科 [4]山西医科大学第一临床学院
出 处:《当代医学》2012年第14期1-3,共3页Contemporary Medicine
摘 要:目的探讨七氟烷后处理对大鼠脑缺血再灌注损伤的保护作用及血红素氧合酶-(1HO-1)的抗炎作用。方法清洁级雄性SD大鼠40只,体重230~270g,随机分为5组,假手术组(C组)、缺血再灌注组(IR组)、七氟烷组(S组)、抑制剂组(S+Z组)和溶剂对照组(S+D组)。采用双侧颈总动脉夹闭合并低血压方法制备脑缺血再灌注损伤模型。将所有大鼠再灌注24h后处死,取海马。光镜下观察各组海马病理学变化,检测海马肿瘤坏死因子α(TNFα)、白细胞介素1β(IL-1β)和HO-1表达。结果七氟烷组HO-1(0.466±0.041)较缺血再灌注组(0.338±0.023)显著升高(P<0.05),TNF-α和IL-1β较缺血再灌注组显著降低(P<0.05);抑制剂组HO-1较七氟烷组显著降低(P<0.05),TNF-α和IL-1β较缺血再灌注组显著升高(P<0.05);七氟烷组海马病理学损伤较缺血再灌注组和抑制剂组减轻。结论七氟烷后处理对大鼠脑缺血再灌注损伤有保护作用,其作用机制可能与七氟烷上调脑组织中HO-1表达,从而抑制炎症反应有关。Objective To investigate the protection of sevoflurane postconditioning on cerebral ischemia-reperfusion injury in rats and heme oxygenase-1(HO-1)after sevoflurane induction of anti-inflammatory role.Methods 40 male SD rats of clean grade weighing 230~270g were randomly divided into 5 groups,and every group was 8 rats.Sham operation group(group C),Ischemia and reperfusion group(group IR),sevoflurane group(group S),inhibitor group(group S+Z)and solvent control group(group S+D).The occlusion of bilateral carotid arteries of 20 minutes combined with hypotension method to establish the model of cerebral ischemia.After reperfution 24 hours,all of the rats were sacrificed and the hippocampus were got.Under light-microscopy pathological changes of every group hippocampus were observed,and TNF-α,IL-1β and HO-1 content were detected.Results Sevoflurane group HO-1(0.466±0.041)compared with ischemia and reperfusion(0.338±0.023)were significantly higher(P0.05),TNF-α and IL-1β compared with ischemia-reperfusion group was significantly lower(P0.05);inhibitor group HO-1 compared with sevoflurane group was significantly lower(P0.05),TNF-α and IL-1β compared with ischemia-reperfusion group was significantly increased(P0.05);The pathological damage of hippocampal in sevoflurane group reduced comparing with that in ischemia reperfusion group and inhibitor group.Conclusion Sevoflurane postconditioning on rat cerebral ischemia-reperfusion has a protective effect,its mechanism may be related to sevoflurane increased brain expression of HO-1,thus inhibiting the inflammatory response.
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