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首页> 外文期刊>Brain research bulletin >Microglial ecto-Ca(2+)-ATPase activity in a rat model of focal homologous blood clot embolic cerebral ischemia: an enzyme histochemical study.
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Microglial ecto-Ca(2+)-ATPase activity in a rat model of focal homologous blood clot embolic cerebral ischemia: an enzyme histochemical study.

机译:小胶质细胞外-Ca(2 +)-ATPase活性的局灶性同源血块栓塞性脑缺血大鼠模型中:酶组织化学研究。

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Post-ischemic changes in ecto-Ca(2+)-ATPase activity in microglia and the infarcted tissue were studied in a rat model of focal embolic cerebral ischemia using an enzyme histochemical method. Ecto-Ca(2+)-ATPase activity was observed in whole brains in non-operated and sham-operated control animals. In addition, this enzyme activity was determined to be localized in ramified microglia. At 30 min after ischemia, non-microglial ecto-Ca(2+)-ATPase activity in the infarcted tissue slightly decreased and continued to decrease thereafter. The ecto-Ca(2+)-ATPase activity in microglia did not appear changed at this time. The decrease of enzyme activity in the infarcted tissue made it much easier to clearly observe ecto-Ca(2+)-ATPase-positive microglia. The enzyme activity of microglia in the ischemic area began to decrease 2 or 4h after embolization and remarkably decreased, except in the perinuclear cytoplasm, apical parts of the processes, and several parts along the processes, 8h after ischemia. By 12h afteronset of embolization, the enzyme activity of microglia and infarcted tissue had almost completely disappeared. Ecto-Ca(2+)-ATPase of microglia is likely to play an important role in the metabolism of extracellular nucleotides in the ischemic area immediately after the onset of embolization by means of ecto-enzymes. Thus, the findings of the present study suggest that microglia might serve to protect the infarcted tissue in the ischemic brain.
机译:在局灶性栓塞性脑缺血的大鼠模型中,使用酶组织化学方法研究了小胶质细胞和梗塞组织中外钙Ca(2 +)-ATPase活性的缺血后变化。在非手术和假手术的对照动物的全脑中观察到Ecto-Ca(2 +)-ATPase活性。另外,确定该酶活性位于分支的小胶质细胞中。缺血后30分钟,梗死组织中的非小胶质细胞外Ca-(2 +)-ATPase活性略有下降,此后继续下降。此时小胶质细胞的ecto-Ca(2 +)-ATPase活性未出现变化。梗塞组织中酶活性的降低使得更容易清楚地观察到外Ca(2 +)-ATPase阳性小胶质细胞。栓塞后2或4小时,缺血区域小胶质细胞的酶活性开始下降,并且显着下降,除了在核分裂后8h的核周细胞质,过程的顶端部分以及过程中的几个部分。栓塞后12小时,小胶质细胞和梗塞组织的酶活性几乎完全消失。小胶质细胞的Ecto-Ca(2 +)-ATPase可能在栓塞开始后通过外切酶立即在缺血区域的细胞外核苷酸的代谢中发挥重要作用。因此,本研究的发现表明小胶质细胞可能起到保护缺血性脑梗死组织的作用。

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