Stress Exacerbates Endometriosis Manifestations and Inflammatory Parameters in an Animal Model
Stress Exacerbates Endometriosis Manifestations and Inflammatory Parameters in an Animal Model
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DOI：
10.1177/1933719112438443
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发表时间：
2012-08-01
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;Flores, Idhaliz;Appleyard, Caroline B.
子宫内膜异位症患者有明显的情绪困扰，然而，压力对这种疾病的病理生理学的贡献尚不清楚。我们使用大鼠子宫内膜异位症模型来研究应激对这种疾病发展的影响及其对炎症参数的影响。雌性Sprague-Dawley大鼠连续10天游泳应激，然后通过将子宫角植入靠近肠系膜的位置进行子宫内膜异位症手术诱导（内应激）。假应力组动物仅缝合，无应力组不接受应力方案。在第60天处死时，测量小肠囊泡并评估结肠的肉眼和显微镜损伤。收集结肠组织和腹膜液用于炎性细胞分析。子宫内膜异位症，无论压力，产生了减少中央促肾上腺皮质激素释放因子免疫反应，特别是在海马CA 3亚区。在子宫内膜异位症动物中发现，先前暴露于压力增加了囊泡的数量和严重程度。应激还增加结肠炎症、运动性、髓过氧化物酶水平和肥大细胞数量。总之，在该动物模型中，既往应激可能通过涉及细胞募集（如肥大细胞）、炎症介质释放和海马中下丘脑-垂体轴反应失调的机制促进子宫内膜异位症的发展和严重程度。
Women with endometriosis have significant emotional distress; however, the contribution of stress to the pathophysiology of this disease is unclear. We used a rat model of endometriosis to examine the effects of stress on the development of this condition and its influence on inflammatory parameters. Female Sprague-Dawley rats were subjected to swim stress for 10 consecutive days prior to the surgical induction of endometriosis by suturing uterine horn implants next to the intestinal mesentery (endo-stress). Sham-stress animals had sutures only, and an endo-no stress group was not subjected to the stress protocol. At the time of sacrifice on day 60, endometriotic vesicles were measured and colons assessed for macroscopic and microscopic damage. Colonic tissue and peritoneal fluid were collected for inflammatory cell analysis. Endometriosis, regardless of stress, produced a decrease in central corticotropin-releasing factor immunoreactivity, specifically in the CA3 subregion of the hippocampus. Prior exposure to stress increased both the number and severity of vesicles found in animals with endometriosis. Stress also increased colonic inflammation, motility, myeloperoxidase levels, and numbers of mast cells. In summary, prior stress may contribute to the development and severity of endometriosis in this animal model through mechanisms involving cell recruitment (eg, mast cells), release of inflammatory mediators, and deregulation of hypothalamic-pituitary axis responses in the hippocampus.