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衰老是保护大鼠皮质切片免受氧葡萄糖剥夺诱导损伤的保护因素。

Aging protects rat cortical slices against to oxygen-glucose deprivation induced damage.

机构信息

Faculty of Medicine, Department of Medical Pharmacology, Bahcesehir University, Istanbul, Turkey.

Faculty of Medicine, Department of Internal Medicine, Uludag University, Bursa, Turkey.

出版信息

Int J Neurosci. 2020 Dec;130(12):1183-1191. doi: 10.1080/00207454.2020.1730830. Epub 2020 Feb 24.

DOI:10.1080/00207454.2020.1730830
PMID:32064981
Abstract

In present study, we aimed to clarify effect of aging on the susceptibility of brain tissue to neurodegeneration induced by ischemia. Damage induced by oxygen-glucose deprivation (OGD) followed by reoxygenation (REO) were compared in cortical slices prepared from young (3 months of age) and aged (22-24 months of age) male Sprague Dawley rats. After incubation of the slices in an oxygen and glucose containing control condition, 2,3,5-triphenyl tetrazolium chloride (TTC) staining intensity was found significantly high in aged cortical slices. Although thirty minutes incubation of the slices in OGD medium followed by REO (OGD-REO) caused similar decline in TTC staining in young and aged cortical slices, staining intensity was still significantly higher in the slices prepared from aged animals. Thirty minutes of OGD-REO, on the other hand, also caused more increase in lactate dehydrogenase (LDH) leakage from young slices. While water contents of the slices were almost equal under control condition, it was significantly high in young cortical slices after OGD-REO incubations. In contrary to these findings, OGD and REO caused more increases in S100B output from aged rat cortical slices. S100B levels in brain regions including the cerebral cortex were also found higher in aged rats. All these results indicate that, cortical slices prepared from aged male rats are significantly less responsive to OGD-REO induced alterations. Since protein S100B outputs were almost doubled from aged cortical slices, a possible involvement of this enhanced S100B output seems to be likely.

摘要

在本研究中,我们旨在阐明衰老对缺血引起的脑组织神经变性易感性的影响。比较了从年轻(3 个月龄)和老年(22-24 个月龄)雄性 Sprague Dawley 大鼠制备的皮质切片中由氧葡萄糖剥夺(OGD)后再复氧(REO)引起的损伤。在含有氧气和葡萄糖的对照条件下孵育切片后,发现老年皮质切片中的 2,3,5-三苯基氯化四氮唑(TTC)染色强度显着升高。尽管年轻和老年皮质切片在 OGD 培养基中孵育 30 分钟后再复氧(OGD-REO)导致 TTC 染色相似下降,但在来自老年动物的切片中染色强度仍然显着升高。另一方面,30 分钟的 OGD-REO 也导致来自年轻切片的乳酸脱氢酶(LDH)漏出显着增加。虽然在对照条件下切片的含水量几乎相等,但在 OGD-REO 孵育后年轻皮质切片中的含水量显着升高。与这些发现相反,OGD 和 REO 导致来自老年大鼠皮质切片的 S100B 输出增加更多。包括大脑皮层在内的脑区的 S100B 水平也在老年大鼠中较高。所有这些结果表明,从老年雄性大鼠制备的皮质切片对 OGD-REO 诱导的变化的反应明显降低。由于来自老年皮质切片的 S100B 输出几乎增加了一倍,因此这种增强的 S100B 输出的可能参与似乎是可能的。

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