研究人員發(fā)現(xiàn)亮藍G（BBG）——與常見食用色素藍1號類似的物質(zhì)——能夠保護脊髓受傷的哺乳動物的神經(jīng),。在這種損傷后,，ATP——能夠促進神經(jīng)細胞的信號傳輸——能夠在受傷脊髓周圍大量出現(xiàn)，并且使神經(jīng)細胞處于活躍狀態(tài),。這將導致炎癥和無法逆轉的組織損傷。但是BBG卻能夠跨越具有高度選擇性的血腦屏障，并抑制脊髓神經(jīng)細胞的ATP受體,。在脊髓受傷15分鐘后施用BBG，將能夠防止小鼠的炎癥并促進自愈合過程(如上圖),。但是研究人員指出,，這里還存在副作用。研究人員在7月27日的美國《國家科學院院刊》（PNAS）網(wǎng)絡版上報告了這一發(fā)現(xiàn),。（生物谷Bioon.com）
生物谷推薦原始出處：
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.
