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首页> 外文期刊>Life sciences >Inducible nitric oxide synthase expression in the ischemic core and penumbra after transient focal cerebral ischemia in mice.
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Inducible nitric oxide synthase expression in the ischemic core and penumbra after transient focal cerebral ischemia in mice.

机译：小鼠短暂性局灶性脑缺血后，其在缺血核心和半影区的诱导型一氧化氮合酶表达。

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The present observations examined the hypothesis that the iNOS expression in the ischemic penumbra after a transient focal ischemic insult is involved in the recruitment of penumbra into infarction. The middle cerebral artery in mice was occluded for 2 h by an intraluminal filament and then recirculated. The measurement of iNOS activity, iNOS protein formation and NO concentration in the ischemic core and penumbra, and the determination of infarct volume were performed at 6, 12, 24 and 48 h after reperfusion. iNOS protein and iNOS enzymatic activity appeared at 6 h, peaked at 24 h, and declined at 48 h in the penumbra after reperfusion. iNOS protein was not detectable in contralateral area and in sham-operated brains. The time course of iNOS protein, enzymatic activity and NO concentration in the penumbra but not in the core matched the process of infarct maturation. Treatment with iNOS inhibitor aminoguanidine (100 mg.kg(-1), i.p.) at 6 and 12 h after reperfusion inhibited iNOS activity by 88.0 +/- 10.4% and reduced NO concentration by 48.5 +/- 8.3% in the penumbra, and lessened infarct size by 48.8 +/- 7.2%. The iNOS activity and NO level in the core were not affected by the administration of aminoguanidine. These results suggest that iNOS expression in the ischemic penumbra is involved in the recruitment of penumbra into infarction and thereby contributing to the enlargement of infarct.
机译：本研究观察了以下假设：短暂性局灶性缺血性损伤后缺血性半影​​中iNOS的表达与半影进入梗死有关。腔内细丝将小鼠的大脑中动脉闭塞2 h，然后再循环。在再灌注后6、12、24和48小时进行iNOS活性，iNOS蛋白形成和缺血核心和半影中NO浓度的测定以及梗塞体积的测定。再灌注后半影中iNOS蛋白和iNOS酶活性在6 h出现，在24 h达到高峰，在48 h下降。在对侧区域和假手术的大脑中均未检测到iNOS蛋白。 iNOS蛋白的时程，半胱氨酸中的酶活性和NO浓度而不是核心中的NO浓度与梗死成熟过程匹配。在再灌注后6和12 h用iNOS抑制剂氨基胍（100 mg.kg（-1），ip）治疗可将iNOS活性抑制88.0 +/- 10.4％，并将半影区的NO浓度降低48.5 +/- 8.3％。梗塞面积减少了48.8 +/- 7.2％。 iNOS活性和核心中的NO水平不受氨基胍给药的影响。这些结果表明，缺血性半影​​中的iNOS表达参与了将半影招募到梗死中，从而有助于梗塞的扩大。

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