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首页> 外文期刊>American Journal of Physiology >Role of epidermal growth factor and its receptor in chemotherapy-induced intestinal injury.
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Role of epidermal growth factor and its receptor in chemotherapy-induced intestinal injury.

机译：表皮生长因子及其受体在化疗诱导的肠道损伤中的作用。

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摘要

Several growth factors are trophic for the gastrointestinal tract and able to reduce the degree of intestinal damage caused by cytotoxic agents. However, studies of epidermal growth factor (EGF) for chemotherapy-induced intestinal injury are conflicting. The development of a transgenic mouse that specifically overexpresses EGF in the small intestine provided a unique opportunity to assess the contribution of EGF in mucositis. After a course of fluorouracil, transgenic mice fared no better than control mice. Weight recovery was inferior, and mucosal architecture was not preserved. Apoptosis was not decreased and proliferation was not increased in the crypts. To corroborate the findings in transgenic mice, ICR mice were treated with exogenous EGF after receiving fluorouracil. Despite ileal upregulation of native and activated EGF receptor, the mice were not protected from intestinal damage. No benefits were observed with different EGF doses or schedules or routes of EGF administration. Finally, mucositiswas induced in mutant mice with specific defects of the EGF signaling axis. Compared with control mice, clinical and histological parameters of intestinal injury after fluorouracil were no different in waved-2 mice, which have functionally diminished EGF receptors, or waved-1 mice, which lack transforming growth factor-alpha, another major ligand for the EGF receptor. These findings do not support a critical role for EGF or its receptor in chemotherapy-induced intestinal injury.
机译：几种生长因子对于胃肠道来说是营养的，并且能够减少由细胞毒剂引起的肠损害的程度。然而，表皮生长因子（EGF）用于化学疗法诱发的肠道损伤的研究存在矛盾。特异性在小肠中过度表达EGF的转基因小鼠的发展为评估EGF在粘膜炎中的作用提供了独特的机会。经过一个疗程的氟尿嘧啶后，转基因小鼠的表现并不比对照小鼠好。体重恢复较差，并且未保留粘膜结构。隐窝中细胞凋亡没有减少，增殖也没有增加。为了证实转基因小鼠的发现，接受氟尿嘧啶后用外源性EGF处理ICR小鼠。尽管回肠天然和激活的EGF受体回肠上调，小鼠没有受到肠道损害的保护。使用不同的EGF剂量或EGF给药时间表或途径未观察到益处。最后，在具有EGF信号传导轴特定缺陷的突变小鼠中诱发粘膜炎。与对照组小鼠相比，氟尿嘧啶引起的肠损伤的临床和组织学参数在功能上减弱了EGF受体的wave-2小鼠或缺乏转化生长因子-α（EGF的另一主要配体）的wave-1小鼠中无差异。受体。这些发现不支持EGF或其受体在化疗诱导的肠道损伤中的关键作用。

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