Lima Rafael R, Santana Luana N S, Fernandes Rafael M, Nascimento Elder M, Oliveira Ana Carolina A, Fernandes Luanna M P, Dos Santos Enio Mauricio N, Tavares Patrycy Assis N, Dos Santos Ijair Rogério, Gimarães-Santos Adriano, Gomes-Leal Walace
Institute of Biological Sciences, Laboratory of Functional and Structural Biology, Federal University of Pará, 66075-900 Belém, PA, Brazil.
Institute of Biological Sciences, Laboratory of Experimental Neuroprotection and Neuroregeneration, Federal University of Pará, 66075-900 Belém, PA, Brazil.
Oxid Med Cell Longev. 2016;2016:3173564. doi: 10.1155/2016/3173564. Epub 2016 Dec 5.
Stroke is a leading cause of death and neurological disability worldwide and striatal ischemic stroke is frequent in humans due to obstruction of middle cerebral artery. Several pathological events underlie damage progression and a comprehensive description of the pathological features following experimental stroke in both acute and chronic survival times is a necessary step for further functional studies. Here, we explored the patterns of microglial activation, astrocytosis, oligodendrocyte damage, myelin impairment, and Nogo-A immunoreactivity between 3 and 30 postlesion days (PLDs) after experimental striatal stroke in adult rats induced by microinjections of endothelin-1 (ET-1). The focal ischemia induced tissue loss concomitant with intense microglia activation between 3 and 14 PLDs (maximum at 7 PLDs), decreasing afterward. Astrocytosis was maximum around 7 PLDs. Oligodendrocyte damage and Nogo-A upregulation were higher at 3 PLDs. Myelin impairment was maximum between 7 and 14 PLDs. Nogo-A expression was higher in the first week in comparison to control. The results add important histopathological features of ET-1 induced stroke in subacute and chronic survival times. In addition, the establishment of the temporal evolution of these neuropathological events is an important step for future studies seeking suitable neuroprotective drugs targeting neuroinflammation and white matter damage.
中风是全球范围内导致死亡和神经功能残疾的主要原因，由于大脑中动脉阻塞，纹状体缺血性中风在人类中很常见。损伤进展有多种病理事件作为基础，全面描述实验性中风后急性和慢性存活期的病理特征是进一步进行功能研究的必要步骤。在此，我们探究了成年大鼠经微量注射内皮素-1（ET-1）诱导实验性纹状体中风后3至30个损伤后天数（PLD）之间小胶质细胞激活、星形胶质细胞增生、少突胶质细胞损伤、髓鞘损伤和Nogo-A免疫反应性的模式。局灶性缺血导致组织损失，同时在3至14个PLD之间小胶质细胞强烈激活（在7个PLD时达到峰值），随后逐渐减少。星形胶质细胞增生在7个PLD左右达到峰值。少突胶质细胞损伤和Nogo-A上调在3个PLD时更高。髓鞘损伤在7至14个PLD之间达到峰值。与对照组相比，Nogo-A表达在第一周更高。这些结果增加了ET-1诱导的中风在亚急性和慢性存活期的重要组织病理学特征。此外，确定这些神经病理事件的时间演变是未来寻求针对神经炎症和白质损伤的合适神经保护药物研究的重要一步。
