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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Intracerebral chondroitinase ABC and heparan sulfate proteoglycan glypican improve outcome from chronic stroke in rats
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Intracerebral chondroitinase ABC and heparan sulfate proteoglycan glypican improve outcome from chronic stroke in rats

机译：脑内软骨素酶ABC和硫酸乙酰肝素蛋白聚糖Glypican改善大鼠慢性中风的预后

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摘要

Physical and chemical constraints imposed by the periinfarct glial scar may contribute to the limited clinical improvement often observed after ischemic brain injury. To investigate the role of some of these mediators in outcome from cerebral ischemia, we treated rats with the growth-inhibitory chondroitin sulfate proteoglycan neurocan, the growth-stimulating heparan sulfate proteoglycan glypican, or the chondroitin sulfate proteoglycan-degrading enzyme chondroitinase ABC. Neurocan, glypican, or chondroitinase ABC was infused directly into the infarct cavity for 7 d, beginning 7 d after middle cerebral artery occlusion. Glypican and chondroitinase ABC reduced glial fibrillary acidic protein immunoreactivity and increased microtubule-associated protein-2 immunoreactivity in the periinfarct region, and glypican- and chondroitinase ABC-treated rats showed behavioral improvement compared with neurocan- or saline-treated rats. Glypican and chondroitinase ABC also increased neurite extension in cortical neuron cultures. Glypican increased fibroblast growth factor-2 expression and chondroitinase ABC increased brain-derived neuro-trophic factor expression in these cultures, whereas no such effects were seen following neurocan treatment. Thus, treatment with glypican or enzymatic disruption of neurocan with chondroitinase ABC improves gross anatomical, histological, and functional outcome in the chronic phase of experimental stroke in rats. Changes in growth factor expression and neuritogenesis may help to mediate these effects.
机译：梗塞周围神经胶质瘢痕强加的物理和化学限制可能导致缺血性脑损伤后经常观察到的有限的临床改善。为了研究某些介体在脑缺血预后中的作用，我们用抑制生长的硫酸软骨素蛋白聚糖神经聚糖，刺激生长的硫酸乙酰肝素蛋白聚糖聚糖或硫酸软骨素降解蛋白软骨素酶ABC来治疗大鼠。从大脑中动脉闭塞7 d开始，将Neurocan，glypican或软骨素酶ABC直接注入梗死腔中7 d。 Glypican和软骨素酶ABC降低了梗塞周围区域的神经胶质纤维酸性蛋白免疫反应性，并增加了微管相关的Protein-2免疫反应性，与神经碱或盐处理的大鼠相比，Glypican和软骨素酶ABC的治疗小鼠的行为改善。 Glypican和软骨素酶ABC在皮质神经元培养物中也增加了神经突的延伸。在这些培养物中，Glypican增加了成纤维细胞生长因子2的表达，而软骨素酶ABC则增加了脑源性神经营养因子的表达，而神经罐治疗后未见此类作用。因此，在大鼠实验性卒中的慢性期中，用软骨素酶ABC给予Glypican或酶破坏神经罐的方法可改善大鼠实验性卒中慢性期的总体解剖学，组织学和功能结果。生长因子表达和神经形成的变化可能有助于介导这些作用。

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