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Stress and Gene Expression of Individuals With Chronic Abdominal Pain

机译:慢性腹痛患者的应激和基因表达

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Background: Research examining the role of stress in gastrointestinal (GI) symptoms such as chronic abdominal pain (CAP) is controversial. The purpose of this study was to examine the expression of genes involved in metabolic stress and toxicity in men and women with high and low levels of perceived stress with and without CAP. Methods: Data and samples were collected and the expression of genes involved in metabolic stress and toxicity was analyzed in 26 individuals who had consented to participate in a natural history protocol. Subjects completed the 10-item Perceived Stress scale (PSS). Fasting participants' peripheral whole blood was collected for proteomic and genomic studies. Polymerase chain reaction (PCR) array was used to analyze the expression of 84 key genes involved in human stress and toxicity plus 5 housekeeping genes. Plasma interleukin-1 alpha (IL-1α) protein was quantified via enzyme-linked immunosorbent assay (ELISA). Results: Interleukin-1 alpha gene (IL1A) was upregulated in females with high stress versus females with low stress by 2.58-fold (95% CI [0.88, 4.28]). IL1A was upregulated in participants with high stress and CAP versus those with low stress and CAP by 3.47-fold (95% CI [1.14, 5.80]). Conclusions: An upregulation of the gene coding the pro-inflammatory cytokine IL-1α suggests that the mechanism behind stress-related changes in GI symptoms is pro-inflammatory in nature. The results of this study contribute to the knowledge of the mechanism behind stress-related CAP symptoms and gender differences associated with these disorders.
机译:背景:有关研究压力在胃肠道(GI)症状(例如慢性腹痛(CAP))中的作用的研究存在争议。这项研究的目的是检查在有和没有CAP的男女中,无论在高低应激压力下,男性和女性的代谢应激和毒性相关基因的表达。方法:收集26名同意参加自然史研究的个体的数据和样本,分析涉及代谢应激和毒性的基因的表达。受试者完成了10个项目的感知压力量表(PSS)。空腹参与者的外周全血被收集用于蛋白质组学和基因组研究。聚合酶链反应(PCR)阵列用于分析涉及人类压力和毒性的84个关键基因的表达以及5个管家基因。血浆白细胞介素-1α(IL-1α)蛋白通过酶联免疫吸附测定(ELISA)进行定量。结果:高压力女性相对低压力女性的白细胞介素-1α基因(IL1A)上调了2.58倍(95%CI [0.88,4.28])。与低压力和CAP的参与者相比,高压力和CAP的参与者的IL1A上调了3.47倍(95%CI [1.14,5.80])。结论:促炎细胞因子IL-1α编码基因的上调表明,与应激有关的胃肠道症状改变的机制本质上是促炎的。这项研究的结果有助于了解与压力相关的CAP症状和与这些疾病相关的性别差异背后的机制。

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