研究人员发现亮蓝G（BBG）——与常见食用色素蓝1号类似的物质——能够保护脊髓受伤的哺乳动物的神经。在这种损伤后，ATP——能够促进神经细胞的信号传输——能够在受伤脊髓周围大量出现，并且使神经细胞处于活跃状态。这将导致炎症和无法逆转的组织损伤。但是BBG却能够跨越具有高度选择性的血脑屏障，并抑制脊髓神经细胞的ATP受体。在脊髓受伤15分钟后施用BBG，将能够防止小鼠的炎症并促进自愈合过程(如上图)。但是研究人员指出，这里还存在副作用。研究人员在7月27日的美国《国家科学院院刊》（PNAS）网络版上报告了这一发现。（生物谷Bioon.com）
生物谷推荐原始出处：
PNAS doi: 10.1073/pnas.0902531106
Systemic administration of an antagonist of the ATP-sensitive receptor P2X7 improves recovery after spinal cord injury
Weiguo Penga,1, Maria L. Cotrinaa,1, Xiaoning Hana, Hongmei Yua, Lane Bekara, Livnat Bluma, Takahiro Takanoa, Guo-Feng Tiana, Steven A. Goldmanb,2 and Maiken Nedergaarda,3
Traumatic spinal cord injury is characterized by an immediate, irreversible loss of tissue at the lesion site, as well as a secondary expansion of tissue damage over time. Although secondary injury should, in principle, be preventable, no effective treatment options currently exist for patients with acute spinal cord injury (SCI). Excessive release of ATP by the traumatized tissue, followed by activation of high-affinity P2X7 receptors, has previously been implicated in secondary injury, but no clinically relevant strategy by which to antagonize P2X7 receptors has yet, to the best of our knowledge, been reported. Here we have tested the neuroprotective effects of a systemically administered P2X7R antagonist, Brilliant blue G (BBG), in a weight-drop model of thoracic SCI in rats. Administration of BBG 15 min after injury reduced spinal cord anatomic damage and improved motor recovery without evident toxicity. Moreover, BBG treatment directly reduced local activation of astrocytes and microglia, as well as neutrophil infiltration. These observations suggest that BBG not only protected spinal cord neurons from purinergic excitotoxicity, but also reduced local inflammatory responses. Importantly, BBG is a derivative of a commonly used blue food color (FD&C blue No. 1), which crosses the blood–brain barrier. Systemic administration of BBG may thus comprise a readily feasible approach by which to treat traumatic SCI in humans.
