2015年8月25日訊/生物谷BIOON/--新研究發現對抗致命的輻射有了新突破。在核輻射暴露後24小時內，一種再生肽可以幫助顯著提高小鼠的生存時間。目前這項研究出版在自然出版集團的雜誌《Laboratory Investigation》上。
德州大學醫學分部研究作者Carla Kantara是生物化學和分子生物學博士後，他說當小鼠處於致命輻射中24小時內單次注入肽類藥物TP508似乎可以大大增加小鼠生存並延遲死亡。
核事故的威脅可能殺死或傷害成千上萬的人，該事故引起全球認知，在接觸核輻射後一天或更多時間後急需醫療措施防止輻射損傷身體並讓人們繼續生存。
暴露於高劑量的輻射可引發一系列潛在的致命影響。這些影響最嚴重的是胃腸道，或胃腸道毒性症候群，是由輻射誘導引起的腸道黏膜的破損。這種類型的胃腸道損傷減少身體吸收水分的能力，導致電解質失衡，引起細菌感染、腸漏、敗血症甚至死亡。
胃腸道毒性症候群是由輻射誘導損傷小腸和結腸中的隱窩上皮細胞，為了胃腸道的正常工作該細胞必須不斷得到補充。隱窩上皮細胞特別容易受到輻射損傷，它可作為指示器檢驗在人體全身輻射暴露後可是否生存。
「目前缺乏可用的治療方法能夠有效地預防輻射誘導的損傷，這促使人們努力尋找可以減少輻射暴露後影響的對策，促使加速被輻射的個人組織修復並增加核事件後生存機會。」 Darrell Carney說，「因為輻射導致損傷的腸道對一個人如何從輻射中復甦起關鍵作用，開發新型藥物能夠預防胃腸道損傷是至關重要的。」
多肽藥物TP508開發用於刺激修復皮膚，骨骼和肌肉組織。以往的經驗顯示，通過刺激適當的血液流動可使組織修復，減少炎症和減少細胞死亡。
「目前的研究結果表明，肽可能是一個有效的緊急核對策略，受害者可以在24小時內的暴露中增加生存率並延遲死亡，可以給受害者在到達醫院之前一定的生命時間。」Kantara說。（生物谷Bioon.com）
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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.