Department of Anatomy & Neurobiology, 72 E. Concord Street, L-1004, Boston University School of Medicine, Boston, MA 02118, USA.
Department of Anatomy & Neurobiology, 72 E. Concord Street, L-1004, Boston University School of Medicine, Boston, MA 02118, USA.
Brain Res. 2019 Aug 15;1717:147-159. doi: 10.1016/j.brainres.2019.04.015. Epub 2019 Apr 15.
Cortical injury elicits long-term cytotoxic and cytoprotective mechanisms within the brain and the balance of these pathways can determine the functional outcome for the individual. Cytotoxicity is exacerbated by production of reactive oxygen species, accumulation of iron, and peroxidation of cell membranes and myelin. There are currently no neurorestorative treatments to aid in balancing the cytotoxic and cytoprotective mechanisms following cortical injury. Cell based therapies are an emerging treatment that may function in immunomodulation, reduction of secondary damage, and reorganization of surviving structures. We previously evaluated human umbilical tissue-derived cells (hUTC) in our non-human primate model of cortical injury restricted to the hand area of primary motor cortex. Systemic hUTC treatment resulted in significantly greater recovery of fine motor function compared to vehicle controls. Here we investigate the hypothesis that hUTC treatment reduces oxidative damage and iron accumulation and increases the extent of the microglial response to cortical injury. To test this, brain sections from these monkeys were processed using immunohistochemistry to quantify oxidative damage (4-HNE) and activated microglia (LN3), and Prussian Blue to quantify iron. hUTC treated subjects exhibited significantly reduced oxidative damage in the sublesional white matter and iron accumulation in the perilesional area as well as a significant increase in the extent of activated microglia along white matter pathways. Increased perilesional iron accumulation was associated with greater perilesional oxidative damage and larger reconstructed lesion volume. These findings support the hypothesis that systemic hUTC administered 24 h after cortical damage decreases the cytotoxic response while increasing the extent of microglial activation.
皮质损伤会在大脑内引发长期的细胞毒性和细胞保护机制,而这些途径的平衡可以决定个体的功能结果。活性氧的产生、铁的积累、细胞膜和髓磷脂的过氧化会加剧细胞毒性。目前,没有神经修复治疗方法可以帮助平衡皮质损伤后的细胞毒性和细胞保护机制。基于细胞的治疗是一种新兴的治疗方法,可能具有免疫调节、减少二次损伤和重建存活结构的功能。我们之前在我们的非人类灵长类皮质损伤模型中评估了人脐带组织来源的细胞(hUTC),该模型仅限于初级运动皮质的手部区域。系统的 hUTC 治疗与载体对照相比,显著提高了精细运动功能的恢复。在这里,我们假设 hUTC 治疗可以减少氧化损伤和铁积累,并增加小胶质细胞对皮质损伤的反应程度。为了验证这一点,我们使用免疫组织化学对这些猴子的脑切片进行了处理,以定量氧化损伤(4-HNE)和激活的小胶质细胞(LN3),并使用普鲁士蓝定量铁。hUTC 治疗组在亚损伤白质中表现出氧化损伤显著减少,在损伤周围区域铁积累减少,以及沿白质通路激活的小胶质细胞数量显著增加。损伤周围铁积累的增加与损伤周围氧化损伤的增加和重建损伤体积的增加有关。这些发现支持这样的假设,即皮质损伤后 24 小时给予系统的 hUTC 可以减少细胞毒性反应,同时增加小胶质细胞激活的程度。