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作 者:关望[1] 王海英[1] 陈志芳[1] 关岚[1] 李天水[1] 金红方[2] 赵斌[1] 杜军保[2]
机构地区:[1]北京积水潭医院,100035 [2]北京大学第一医院儿科,100034
出 处:《当代医学》2010年第18期7-8,共2页Contemporary Medicine
摘 要:目的观察外源性硫化氢对急性肺损伤大鼠氧化应激的调节作用。方法雄性SD大鼠18只,随机分为对照组(n=6)、油酸组(OA,n=6)、OA+硫氢化钠(NaHS)组(n=6)。OA组鼠尾静脉注射油酸0.1ml/kg;OA+NaHS组先腹腔注射NaHS56umol/kg,30min后再尾静脉注射油酸0.1ml/kg。对照组鼠尾静脉注射0.1ml/Kg生理盐水。以上3组观察6h后处死动物。观察指标:支气管肺泡灌洗液(BALF)沉渣行白细胞分类计数;肺损伤的组织学半定量评分;测定肺组织匀浆中H2S含量;超氧化物岐化酶(SOD)和丙二醛(MDA)的含量。结果 OA组与对照组比,光镜下肺组织明显受损,中性粒细胞(PMN)计数和肺损伤评分明显增高(P<0.05或<0.01);肺组织匀浆中H2S明显降低(P<0.01);MDA显著增加(P<0.05);SOD显著降低(P<0.05);OA+NaHS组肺损伤程度减轻;与OA组比肺组织匀浆中H2S明显升高(P<0.05);MDA含量显著降低,SOD含量显著升高(P均<0.05)。结论补充H2S可减轻氧化应激反应,进而对急性肺损伤大鼠产生保护作用。Objective To exploring the regulative effects of exogenously applied hydrogen sulfide(H2S) on oxidative stress in acute lung injury(ALI) in rats.Methods Eighteen male SD rats were randomly divided into control group(n=6),OA group(n=6) and OA+sodium hydrosulfide(NaHS) group(n=6).ALI was induced by injecting oleic acid(0.1ml/kg) intravenously as OA group;controls were given normal saline(0.1ml/kg);NaHS solution(56μmol/kg) was injected intraperitoneally 30 min before OA(0.1ml/kg) injection as OA+NaHS group.OA group and OA+NaHS group were executed at 6 h after the administration of OA,respectively.Control group was executed at 6 hours after receiving intravenous normal saline.The measured indexes include counts of PMN in BALF and IQA score.The concentrations of H2S and the levels of SOD,MDA in lung tissue were assayed respectively.Results Compared with control group,severe injuries of lung tissues were observed in rats treated with OA.In addition,significantly increased MDA levels together with decreased SOD,H2S levels were observed in the lung tissue of OA-treated rats compared to controls(P0.01 or P0.05).Administration of NaHS before OA could lessen the lung pathologic changes induced by OA,elevate the concentrations of H2S and SOD in lung tissues(P0.05),but the level of MDA decreased significantly(P0.05).Conclusion Exogenous H2S could attenuate oxidative stress and therefore plays a protective role in oleic acid induced ALI in rats.
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