Purpose: Gastrointestinal (GI) injuries post ionizing radiation (IR) becomes a crucial factor in survival. Thus, the current study was aimed to explore the molecular mechanisms behind IR produced GI proteome alterations and their amelioration by a safe radioprotective formulation candidate, G-003M (podophyllotoxin+rutin).

Materials and method: C57BL/6 mice were administered with G-003M 1 h before 9 Gy whole body γ irradiation. 2DE-MS analysis was conducted to identify differential expression of jejunum proteins with fold change >1.5 (p < .05) at various time-points.

Results: G-003M pre-administration decreased total number of differential proteins. It mediated protection to cytoskeleton, modulated stress, apoptosis and inflammatory proteins. Direct effect on eukaryotic translation initiation factor 4H (Eif4h), thioredoxin domain-containing protein 17 (Txndc17) and interferon-induced protein 35 (Ifi35) was observed. Bioinformatics depicted transcription factor-MYC, was also positively modulated by G-003M. Further, it also enhanced level of citrulline (ELISA analysis), and restored crypts and villi lengths (histological analysis) against severe damage caused by lethal irradiation.

Conclusion: Current findings reveal that G-003M may be an efficient candidate in protecting key proteins of metabolic and biochemical pathways assisting in the rapid recovery of GI proteome. This fairly improved the chances of animal survival exposed to lethal doses of whole body radiation.

目的：电离辐射（IR）后胃肠道（GI）损伤成为生存的关键因素。因此，当前的研究旨在探索IR产生的GI蛋白质组改变背后的分子机制，以及通过安全的放射防护配方候选物G-003M（鬼臼毒素+芦丁）来改善它们的机制。

材料和方法： C57BL / 6小鼠在9 Gy全身γ射线照射前1 h给予G-003M。进行2DE-MS分析以鉴定空肠蛋白 在不同时间点的倍数变化> 1.5（p <.05）的差异表达。

结果： G-003M的预给药减少了差异蛋白的总数。它介导了对细胞骨架，调节的应激，凋亡和炎症蛋白的保护。观察到对真核翻译起始因子4H（Eif4h），含硫氧还蛋白域的蛋白17（Txndc17）和干扰素诱导的蛋白35（Ifi35）的直接影响。生物信息学描述了转录因子-MYC，也受到G-003M的正调控。此外，它还增强了瓜氨酸的水平（ELISA分析），并恢复了隐窝和绒毛长度（组织学分析），以抵抗由致命辐射引起的严重损害。

结论：目前的发现表明，G-003M可能是保护代谢和生化途径关键蛋白的有效候选者，从而有助于GI蛋白质组的快速恢复。相当剂量地暴露于致死剂量的全身辐射下，动物存活的机会增加了。