Liu Nai-Wei, Ke Chien-Chih, Zhao Yonghua, Chen Yi-An, Chan Kim-Chuan, Tan David Tat-Wei, Lee Jhih-Shian, Chen You-Yin, Hsu Tun-Wei, Hsieh Ya-Ju, Chang Chi-Wei, Yang Bang-Hung, Huang Wen-Sheng, Liu Ren-Shyan
State Key Laboratory of Quality Research in Chinese Medicine, Faculty of Chinese Medicine, Macau University of Science and Technology, Avenida Wai Long, Taipa, 999078, Macau.
Biomedical Imaging Research Center, National Yang-Ming University, Taipei, Taiwan.
Transl Stroke Res. 2017 Jun;8(3):244-256. doi: 10.1007/s12975-016-0512-4. Epub 2016 Dec 1.
Photochemically induced cerebral ischemia is an easy-manipulated, reproducible, relatively noninvasive, and lesion controllable model for translational study of ischemic stroke. In order to longitudinally investigate the characterization of the model, magnetic resonance imaging, F-2-deoxy-glucose positron emission tomography, fluorescence, and bioluminescence imaging system were performed in correlation with triphenyl tetrazolium chloride (TTC), hematoxylin-eosin staining, and immunohistochemistry examinations of glial fibrillary acidic protein, CD68, NeuN, von willebrand factor, and α-smooth muscle actin in the infarct zone. The results suggested that the number of inflammatory cells, astrocytes, and neovascularization significantly elevated in peri-infarct region from day 7 and a belt of macrophage/microglial and astrocytes was formed surrounding infarct lesion at day 14. Both vasogenic and cytotoxic edema, as well as blood brain-barrier leakage, occurred since day 1 after stroke induction and gradually attenuated with time. Numerous cells other than neuronal cells infiltrated into infarct lesion, which resulted in no visible TTC negative regional existence at day 14. Furthermore, recovery of cerebral blood flow and glucose utilization in peri-infarct zone were noted and more remarkably than that in infarct core following the stroke progression. In conclusion, these characterizations may be highly beneficial to the development of therapeutic strategies for ischemic stroke.
光化学诱导的脑缺血是一种易于操作、可重复、相对无创且病变可控的模型,用于缺血性中风的转化研究。为了纵向研究该模型的特征,进行了磁共振成像、F-2-脱氧葡萄糖正电子发射断层扫描、荧光和生物发光成像系统,并与梗死区的氯化三苯基四氮唑(TTC)、苏木精-伊红染色以及胶质纤维酸性蛋白、CD68、NeuN、血管性血友病因子和α-平滑肌肌动蛋白的免疫组织化学检查相关联。结果表明,从第7天起,梗死周边区域的炎性细胞、星形胶质细胞数量和新生血管形成显著增加,在第14天时,梗死灶周围形成了一圈巨噬细胞/小胶质细胞和星形胶质细胞带。自中风诱导后第1天起,血管源性和细胞毒性水肿以及血脑屏障渗漏均出现,并随时间逐渐减轻。除神经元细胞外,大量细胞浸润到梗死灶中,导致在第14天时没有可见的TTC阴性区域存在。此外,在中风进展后,梗死周边区域的脑血流和葡萄糖利用有所恢复,且比梗死核心区域更明显。总之,这些特征可能对缺血性中风治疗策略的开发非常有益。