新研究发现对抗致命的辐射有了新突破。在核辐射暴露后24小时内，一种再生肽可以帮助显著提高小鼠的生存时间。目前这项研究出版在自然出版集团的杂志《Laboratory Investigation》上。

　　德州大学医学分部研究作者Carla Kantara是生物化学和分子生物学博士后，他说当小鼠处于致命辐射中24小时内单次注入肽类药物TP508似乎可以大大增加小鼠生存并延迟死亡。

　　核事故的威胁可能杀死或伤害成千上万的人，该事故引起全球认知，在接触核辐射后一天或更多时间后急需医疗措施防止辐射损伤身体并让人们继续生存。

　　暴露于高剂量的辐射可引发一系列潜在的致命影响。这些影响最严重的是胃肠道，或胃肠道毒性综合征，是由辐射诱导引起的肠道粘膜的破损。这种类型的胃肠道损伤减少身体吸收水分的能力，导致电解质失衡，引起细菌感染、肠漏、败血症甚至死亡。

　　胃肠道毒性综合征是由辐射诱导损伤小肠和结肠中的隐窝上皮细胞，为了胃肠道的正常工作该细胞必须不断得到补充。隐窝上皮细胞特别容易受到辐射损伤，它可作为指示器检验在人体全身辐射暴露后可是否生存。

　　“目前缺乏可用的治疗方法能够有效地预防辐射诱导的损伤，这促使人们努力寻找可以减少辐射暴露后影响的对策，促使加速被辐射的个人组织修复并增加核事件后生存机会。” Darrell Carney说，“因为辐射导致损伤的肠道对一个人如何从辐射中复苏起关键作用，开发新型药物能够预防胃肠道损伤是至关重要的。”

　　多肽药物TP508开发用于刺激修复皮肤，骨骼和肌肉组织。以往的经验显示，通过刺激适当的血液流动可使组织修复，减少炎症和减少细胞死亡。

　　“目前的研究结果表明，肽可能是一个有效的紧急核对策略，受害者可以在24小时内的暴露中增加生存率并延迟死亡，可以给受害者在到达医院之前一定的生命时间。”Kantara说。

　　doi:10.1038/labinvest.2015.103

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　　Novel regenerative peptide TP508 mitigates radiation-induced gastrointestinal damage by activating stem cells and preserving crypt integrity

　　Carla Kantara, Stephanie M Moya, Courtney W Houchen, Shahid Umar, Robert L Ullrich, Pomila Singh and Darrell H Carney

　　In recent years, increasing threats of radiation exposure and nuclear disasters have become a significant concern for the United States and countries worldwide. Exposure to high doses of radiation triggers a number of potentially lethal effects. Among the most severe is the gastrointestinal (GI) toxicity syndrome caused by the destruction of the intestinal barrier, resulting in bacterial translocation, systemic bacteremia, sepsis, and death. The lack of effective radioprotective agents capable of mitigating radiation-induced damage has prompted a search for novel countermeasures that can mitigate the effects of radiation post exposure, accelerate tissue repair in radiation-exposed individuals, and prevent mortality. We report that a single injection of regenerative peptide TP508 (rusalatide acetate, Chrysalin) 24 h after lethal radiation exposure (9 Gy, LD100/15) appears to significantly increase survival and delay mortality by mitigating radiation-induced intestinal and colonic toxicity. TP508 treatment post exposure prevents the disintegration of GI crypts, stimulates the expression of adherens junction protein E-cadherin, activates crypt cell proliferation, and decreases apoptosis. TP508 post-exposure treatment also upregulates the expression of DCLK1 and LGR5 markers of stem cells that have been shown to be responsible for maintaining and regenerating intestinal crypts. Thus, TP508 appears to mitigate the effects of GI toxicity by activating radioresistant stem cells and increasing the stemness potential of crypts to maintain and restore intestinal integrity. These results suggest that TP508 may be an effective emergency nuclear countermeasure that could be delivered within 24 h post exposure to increase survival and delay mortality, giving victims time to reach clinical sites for advanced medical treatment.