Intestinal stem cells (ISCs) play a crucial role in maintaining intestinal homeostasis upon chemotherapy and radiotherapy. It has been documented that prostaglandin E2 (PGE2) treatment improved hematopoietic stem cell function in vitro and in vivo, while the relationship between PGE2 and intestinal stem cells remains unclear. Presently, mice were exposed to PGE1, dmPGE2 and indomethacin. Numbers and function of ISCs were assessed by analyzing Olfm4+ ISCs. Intestinal protection of dmPGE2 was investigated on a 5-fluorouracil (5FU)-induced intestinal damage mouse model. The results showed that dmPGE2 treatment, but not PGE1, increased numbers of Olfm4+ ISCs in dose- and time-dependent manners. Indomethacin treatment decreased numbers of Olfm4+ ISCs. The beneficial effects of short-term dmPGE2 treatment on intestine were supported in a 5FU-induced intestinal damage model. Our data showed that 5FU treatment significantly decreased numbers of Olfm4+ ISCs and goblet cells in intestine, which could be ameliorated by dmPGE2 treatment. dmPGE2 treatment accelerated the recovery of 5FU-induced ISC injury via increasing expression of cyclin D1 and D2 in intestine. Furthermore, dmPGE2 treatment-induced expression of cyclin D1 and D2 might be mediated by up-regulation of FOXM1 expression in intestine. These findings feature PGE2 as an effective protector against chemotherapy-induced intestinal damage.

中文翻译：

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前列腺素E2通过增加细胞周期蛋白D的表达来加速化疗诱导的肠道损伤的恢复。

肠道干细胞（ISC）在化学疗法和放射疗法中在维持肠道稳态方面起着至关重要的作用。据报道，前列腺素E2（PGE2）治疗改善了体内和体外的造血干细胞功能，而PGE2与肠干细胞之间的关系仍不清楚。目前，小鼠暴露于PGE1，dmPGE2和消炎痛。通过分析Olfm4 + ISC评估ISC的数量和功能。在5-氟尿嘧啶（5FU）诱导的肠道损伤小鼠模型上研究了dmPGE2的肠道保护作用。结果表明，dmPGE2处理（而非PGE1处理）以剂量和时间依赖性方式增加了Olfm4 + ISC的数量。消炎痛治疗可降低Olfm4 + ISC的数量。短期dmPGE2治疗对肠的有益作用在5FU诱导的肠损伤模型中得到支持。我们的数据显示5FU处理可显着减少肠道中Olfm4 + ISC和杯状细胞的数量，而dmPGE2处理可改善这种情况。dmPGE2处理通过增加肠道中细胞周期蛋白D1和D2的表达来加速5FU诱导的ISC损伤的恢复。此外，dmPGE2处理诱导的细胞周期蛋白D1和D2的表达可能是由肠道FOXM1表达的上调介导的。这些发现将PGE2作为有效的保护剂，可防止化疗引起的肠道损伤。dmPGE2处理通过增加肠道中细胞周期蛋白D1和D2的表达来加速5FU诱导的ISC损伤的恢复。此外，dmPGE2处理诱导的细胞周期蛋白D1和D2的表达可能是由肠道FOXM1表达的上调介导的。这些发现将PGE2作为有效的保护剂，可防止化疗引起的肠道损伤。dmPGE2处理通过增加肠道中细胞周期蛋白D1和D2的表达，加速了5FU诱导的ISC损伤的恢复。此外，dmPGE2处理诱导的细胞周期蛋白D1和D2的表达可能是由肠道FOXM1表达的上调介导的。这些发现将PGE2作为有效的保护剂，可防止化疗引起的肠道损伤。