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Abstract：
Our previous study indicated that sodium orthovanadate (vanadate), a strong inhibitor of p53, effectively suppressed the lethality from the hematopoietic (HP) and gastrointestinal (GI) syndromes after 12 Gy total-body irradiation (TBI) in mice. This conclusion, however, was inconsistent with the fact that p53 plays a radioprotective role in the intestinal epithelium. The death after TBI of around 12 Gy was attributed to a combined effect of HP and GI syndromes. To verify the effect from prophylactic administration of p53 inhibitor on protection of HP and GI syndromes, in this study, the radioprotective effects from vanadate were investigated in TBI and lower half-body irradiation (partial-body irradiation: PBI) mouse models.
Female ICR mice were given a single injection of vanadate or vehicle, followed by a lethal dose of TBI or PBI. Radioprotective effects of vanadate against the irradiations were evaluated by analyzing survival rate, body weight, hematopoietic parameters, and histological changes in the bone marrow and intestinal epithelium.
TBI-induced HP syndrome was effectively suppressed by vanadate treatment. After TBI, the vanadate-treated mice retained better bone marrow cellularity and showed markedly higher survival rate compared to the vehicle-treated animals. In contrast, vanadate did not relieve loss of intestinal crypts and failed to rescue mice from GI death after PBI.
Vanadate is a p53 inhibitor that has been shown to be beneficial as a radiation protective agent against HP but was not effective in protecting against acute GI radiation injury.
Female ICR mice were given a single injection of vanadate or vehicle, followed by a lethal dose of TBI or PBI. Radioprotective effects of vanadate against the irradiations were evaluated by analyzing survival rate, body weight, hematopoietic parameters, and histological changes in the bone marrow and intestinal epithelium.
TBI-induced HP syndrome was effectively suppressed by vanadate treatment. After TBI, the vanadate-treated mice retained better bone marrow cellularity and showed markedly higher survival rate compared to the vehicle-treated animals. In contrast, vanadate did not relieve loss of intestinal crypts and failed to rescue mice from GI death after PBI.
Vanadate is a p53 inhibitor that has been shown to be beneficial as a radiation protective agent against HP but was not effective in protecting against acute GI radiation injury.
摘要：
我们以前的研究表明，原钒酸钠（钒），p53的强抑制剂，有效抑制小鼠在12Gy全身照射（TBI）后造血（HP）和胃肠道（GI）综合征的致死性。这个结论,然而,与p53在肠上皮中起辐射防护作用的事实不一致。TBI后约12Gy的死亡归因于HP和GI综合征的综合作用。为了验证p53抑制剂预防性给药对HP和GI综合征的保护作用。在这项研究中，在TBI和下半体照射（部分体照射：PBI）小鼠模型中研究了钒酸盐的辐射防护作用。
给予雌性ICR小鼠单次注射钒酸盐或赋形剂，然后是致死剂量的TBI或PBI。通过分析存活率评估了钒酸盐对辐射的辐射防护作用，体重,造血参数，骨髓和肠上皮的组织学变化。
钒酸盐治疗可有效抑制TBI诱导的HP综合征。在TBI之后,与媒介物治疗的动物相比,钒酸盐治疗的小鼠保留了更好的骨髓细胞,并显示出明显更高的存活率.相比之下,Vanadate不能减轻肠道隐窝的损失，也未能挽救小鼠在PBI后的胃肠道死亡。
钒酸盐是一种p53抑制剂，已被证明作为抗HP的辐射保护剂是有益的，但在预防急性胃肠道辐射损伤方面无效。
给予雌性ICR小鼠单次注射钒酸盐或赋形剂，然后是致死剂量的TBI或PBI。通过分析存活率评估了钒酸盐对辐射的辐射防护作用，体重,造血参数，骨髓和肠上皮的组织学变化。
钒酸盐治疗可有效抑制TBI诱导的HP综合征。在TBI之后,与媒介物治疗的动物相比,钒酸盐治疗的小鼠保留了更好的骨髓细胞,并显示出明显更高的存活率.相比之下,Vanadate不能减轻肠道隐窝的损失，也未能挽救小鼠在PBI后的胃肠道死亡。
钒酸盐是一种p53抑制剂，已被证明作为抗HP的辐射保护剂是有益的，但在预防急性胃肠道辐射损伤方面无效。
