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机构地区:[1]徐州医学院病理生理学教研室,江苏徐州221002 [2]徐州医学院生理学教研室 [3]徐州医学院神经生物学研究中心
出 处:《徐州医学院学报》2009年第5期298-300,共3页Acta Academiae Medicinae Xuzhou
基 金:国家自然科学基金(30570671);徐州医学院科研课题(08KJ11)
摘 要:目的研究缺血后处理(ischemic post-conditioning,I-postC)对大鼠胃缺血/再灌注(gastric ischemia/reperfusion,GI/R)损伤的影响。方法健康SD大鼠18只,随机分为3组,即对照组、缺血/再灌注组、缺血后处理组,分别检测大鼠胃黏膜损伤指数(GMDI)及胃黏膜组织抑制羟自由基能力、黄嘌呤氧化酶(XOD)、丙二醛(MDA)、超氧化物歧化酶(SOD)含量。结果缺血/再灌注可造成胃黏膜明显损伤;缺血后处理明显减轻GI/R损伤,并使胃黏膜组织抑制羟自由基能力、SOD含量增加,XOD、MDA明显降低。结论缺血后处理减轻大鼠胃缺血/再灌注损伤,其保护机制与减轻缺血/再灌注胃黏膜自由基损伤有关。Objective To investigate the effects and mechanism of ischemic post - conditioning on gastric ischemia -reperfusion (GI/R) - induced injury in rats. Methods 18 Sprague - Dawley rats were randomly divided into 3 groups: the normal group, the GI/R group and the I -postC group. The gastric mucosal damage index (GMDI) and the inhibitory effect of gastric mucosa on hydroxyl free radicals as well as the expression of xanthane oxidase ( XOD), malondialdeilyde (MDA) and superoxide dismutase (SOD) were measured respectively. Results The gastric mucosa was markedly injured after GI/R. Compared with GI/R group, I - postC evidently lessened gastric mucosal damage and enhanced the ability of gastric mucosa against hydroxyl free radicals and up - regulated the expression of SOD and down - regulated the expression of XOD and MDA. Conclusion I - postC can significantly protect against G1/R injury, and the protective mechanism is related to the inhibitory effect of I - postC against free radicals.
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