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暴露于慢性间歇性常压缺氧的大鼠淋巴细胞的白细胞介素表达

Interleukins expression by rat Lymphocytes exposed to chronic intermittent normobaric hypoxia.

作者信息

Calderon-Jofre Rodrigo, Bernal Giuliano, Moraga Daniel, Moraga Fernando A

机构信息

Laboratorio de Fisiología, Hipoxia y Función Vascular, Departamento de Ciencias Biomédicas, Facultad de Medicina, Universidad Católica del Norte, Coquimbo, Chile.

Laboratorio de Biología Molecular y Celular del Cáncer, Departamento de Ciencias Biomédicas, Facultad de Medicina, Universidad Católica del Norte, Coquimbo, Chile.

出版信息

Front Physiol. 2025 Mar 26;16:1520174. doi: 10.3389/fphys.2025.1520174. eCollection 2025.

Abstract

Acute and chronic hypoxia modulate the expression of inflammatory mediators known as cytokines. However, studies in chronic and intermittent hypobaric or normobaric hypoxia, like those described in miner's population, are scarce or absent. In this study, we evaluate the effect of chronic intermittent normobaric hypoxia (CINH) on the hematological response and the expression of lymphocyte cytokines IL-1, IL-2, IL-6, and IL-10 in rats. A total of 20 Sprague-Dawley rats were divided into two groups: a) CINH (FiO 10%, n = 10) and b) Control (normoxic, n = 10). Systolic arterial pressure and heart rate were measured using a tail-cuff sensor. Blood samples were obtained from both groups for hematological studies, and expression of cytokines obtained from lymphocytes was determined by RT-PCR. Hematocrit, hemoglobin, platelet count, and hematological constant were elevated, and leucocyte count decreased in CINH rats. In addition, systolic arterial pressure in CINH rats was significantly increased (over 50%). Cytokine expression from lymphocytes showed that IL-2, and IL-10 increased by 140% and 38%, respectively; IL-6 showed no significant change, while IL-1β expression decreased by 18%. In this regard, CINH could activate an inflammatory response mediated by IL-2. However, this response could be attenuated by increased IL-10 expression, a known anti-inflammatory cytokine, and decreased IL-1β and IL-6 expression, indicative of an adaptation mechanism to CINH.

摘要

急性和慢性缺氧可调节被称为细胞因子的炎症介质的表达。然而,对于慢性和间歇性低压或常压缺氧的研究,如在矿工群体中所描述的那样,却很稀少或几乎没有。在本研究中,我们评估了慢性间歇性常压缺氧(CINH)对大鼠血液学反应以及淋巴细胞细胞因子白细胞介素-1(IL-1)、白细胞介素-2(IL-2)、白细胞介素-6(IL-6)和白细胞介素-10(IL-10)表达的影响。总共20只Sprague-Dawley大鼠被分为两组:a)CINH组(吸入氧分数为10%,n = 10)和b)对照组(常氧,n = 10)。使用尾套传感器测量收缩压和心率。从两组获取血样用于血液学研究,并通过逆转录聚合酶链反应(RT-PCR)测定从淋巴细胞获得的细胞因子的表达。CINH组大鼠的血细胞比容、血红蛋白、血小板计数和血液学常数升高,白细胞计数降低。此外,CINH组大鼠的收缩压显著升高(超过50%)。淋巴细胞的细胞因子表达显示,IL-2和IL-10分别增加了140%和38%;IL-6无显著变化,而IL-1β表达降低了18%。在这方面,CINH可激活由IL-2介导的炎症反应。然而,这种反应可能会因已知的抗炎细胞因子IL-10表达增加以及IL-1β和IL-6表达降低而减弱,这表明是对CINH的一种适应机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4662/11979230/2e988ba82542/fphys-16-1520174-g001.jpg

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