Stress During Development of Experimental Endometriosis Influences Nerve Growth and Disease Progression
Stress During Development of Experimental Endometriosis Influences Nerve Growth and Disease Progression
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DOI：
10.1177/1933719117737846
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发表时间：
2018-03-01
影响因子：
2.9
通讯作者：
Appleyard, Caroline B.
中科院分区：
文献类型：
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作者：
Cuevas, Marielly;Cruz, Myrella L.;Appleyard, Caroline B.
目的：我们之前已经表明，诱导前的应激会恶化子宫内膜异位症大鼠模型的临床表现和炎症参数。本研究旨在探讨子宫内膜异位症发展过程中的压力是否会通过神经生长和免疫改变影响子宫内膜异位植入物的生长。方法：通过将子宫角植入物缝合到小肠系膜上，在雌性 Sprague-Dawley 大鼠中进行手术诱导子宫内膜异位症。两周后，一组大鼠（内应激）接受为期 10 天的游泳应激方案。对照没有应力（内无应力）或仅缝合和应力（假应力）。第60天，处死所有大鼠并检查子宫内膜异位囊泡的存在。测量每个囊泡的大小。切除子宫和结肠，并评估损伤、细胞浸润以及神经生长因子 (NGF)、其受体（p75 和原肌球蛋白受体激酶 A (Trk-A)/pTrk-A）以及降钙素基因相关肽（一种感觉纤维标记物）的表达。对腹膜液白细胞计数进行了差异分析。结果：压力显着增加了子宫内膜异位囊泡的大小，但没有结肠损伤和肥大细胞浸润增加。在接受应激的子宫内膜异位症动物的子宫中发现 NGF 及其受体的表达显着增加。结论：应激刺激子宫内膜异位症动物模型中异位子宫内膜囊泡的发育，并增加炎症细胞向腹膜的募集。此外，压力会促进子宫内神经纤维的生长。
Purpose: We have previously shown that stress prior to induction worsens clinical presentation and inflammatory parameters in a rat model of endometriosis. This study was designed to examine whether stress during the development of endometriosis can affect the growth of endometriotic implants through nerve growth and immune alterations.Methods: Endometriosis was surgically induced in female Sprague-Dawley rats by suturing uterine horn implants onto the small intestine mesentery. Two weeks later, one group of rats (endo-stress) was subjected to a 10-day swim stress protocol. Controls had no stress (endo-no stress) or sutures only and stress (sham-stress). On day 60, all rats were killed and examined for the presence of endometriotic vesicles. The size of each vesicle was measured. The uterus and colon were removed and assessed for damage, cell infiltration, and expression of nerve growth factor (NGF), its receptors (p75 and Tropomyosin receptor kinase A (Trk-A)/pTrk-A), and calcitonin gene-related peptide, a sensory fiber marker. A differential analysis of peritoneal fluid white blood cell count was performed.Results: Stress significantly increased endometriotic vesicle size but not colonic damage and increased infiltration of mast cells. Significantly increased expression of NGF and its receptors was found in the uterus of animals with endometriosis receiving stress.Conclusions: Stress stimulates the development of ectopic endometrial vesicles in an animal model of endometriosis and increases inflammatory cell recruitment to the peritoneum. In addition, stress promotes nerve fiber growth in the uterus.