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作 者:赵胜[1] 沈道江 冯国清[2] 张贺鸣[2] 翁士艾[2]
机构地区:[1]杭州市萧山区妇幼保健院儿科,浙江杭州311201 [2]郑州大学医学院药理教研室,河南郑州450052
出 处:《基础医学与临床》2005年第5期465-467,共3页Basic and Clinical Medicine
摘 要:目的探讨己酮可可碱(pentoxifylline,PTX)对新生大鼠缺氧缺血性脑病(hypoxic-ischemicencephalopathy,HIE)脑组织中ATP酶和炎性细胞因子的影响,揭示PTX对大鼠HIE的保护机制。方法7日龄Wistar大鼠80只随机分为假手术组、缺血组、低氧组、HIE模型组和PTX组。缺血72h后测定脑组织中Na+、K+-ATP酶、Ca2+-ATP酶和Mg2+-ATP酶活性,以及TNF-αI、L-1和TXB2含量。结果缺血组、低氧组和HIE模型组Na+、K+-ATP酶、Ca2+-ATP酶和Mg2+-ATP酶活性降低(P<0.01),TNF-αI、L-1和TXB2含量升高(P<0.05,P<0.01)。PTX组可显著缓解上述变化(P<0.05,P<0.01)。结论PTX对新生大鼠HIE的保护作用可能与其保护脑组织中ATP酶和降低炎性细胞因子有关。ObjectiveTo explore the effects of pentoxifylline(PTX) on ATPase and inflammatory cytokines in cerebral tissue and to identify the mechanism of PTX protection in newborn rats with hypoxic-ischemic encephalopathy. (MethodsWistar) rats(80 case) were randomly divided into sham-operation (Sham) group, ischemia (I) group, hypoxia (H) group, hypoxic-ischemic encephalopathy model (HIE) group and PTX group. After hypoxic-ischemic processing, the activities of Na^+, K^+-ATPase, Ca^(2+)-ATPase and Mg^(2+)-ATPase and the content of TNF-α,IL-1 and TXB_2 in cerebral tissue were measured. ResultsThe activities of Na^+, K^+-ATPase, Ca^(2+)-ATPase and Mg^(2+)-ATPase in the I group,H group and HIE group were significantly decreased and the contents of TNF-α?IL-1 and TXB_2 were markedly increased (P<0.05, P<0.01) as compared to the Sham group. PTX attenuated those changes markedly (P<0.05, P<0.01).ConclusionThe results demonstrate the protective effect of PTX against hypoxic-ischemic encephalopathy in rats which is possibly related to the protection of activities of ATPase to the decreasing of inflammatory cytokines in cerebral tissue.
关 键 词:缺氧缺血性脑病 己酮可可碱 新生大鼠 保护作用 CA^2+-ATP酶 Mg^2+-ATP酶 Wistar大鼠 K^+-ATP酶 炎性细胞因子 TNF-α ATP酶活性 Na^+ TXB2 IL-1 0.05 HIE 脑组织 保护机制 72h后 活性降低 FIX PTX 低氧 模型 含量
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