I H Sever, B Ozkul, D Erisik Tanriover, O Ozkul, C S Elgormus, S G Gur, I Sogut, Y Uyanikgil, E O Cetin, O Erbas
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Rats were randomly assigned into four groups: control group (no procedure was applied, n = 8), untreated septic group [was operated (FIP) and received no treatment, n = 8], placebo group (FIP, treated with 10 ml/kg of saline at once, n = 8), and treated group (FIP, treated with 0.1 mg/kg of oxytocin at once, n = 8). Chest CT was performed for all rats 20 hours after the procedure and density of the lungs were measured manually by using HU. All animals were sacrificed for histopathological examination of lung damage and blood samples were collected for biochemical analysis.</p><p><p>Plasma malondialdehyde (MDA), lactic acid (LA), C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), interleukin 1-beta (IL 1-β) levels were significantly increased in the placebo (FIP + saline) and the untreated (FIP) groups, and plasma levels of all biomarkers were reversed by oxytocin. 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引用次数: 8
摘要
虽然一些研究表明催产素在不同的病理生理过程中具有抗炎作用,但描述催产素对急性呼吸窘迫综合征(ARDS)影响的数据有限。我们的目的是通过组织病理学评估和放射学成像以及生化指标来阐明催产素在ARDS中的保护作用。为建立脓毒症模型,对32只大鼠中的24只进行了粪便腹腔注射(FIP)。将大鼠随机分为4组:对照组(未做任何手术,n = 8)、脓毒症未处理组[已做手术,不做任何治疗,n = 8]、安慰剂组(FIP,一次性给予生理盐水10 ml/kg, n = 8)、治疗组(FIP,一次性给予催产素0.1 mg/kg, n = 8)。术后20小时,所有大鼠均行胸部CT扫描,并用HU手工测量肺密度。所有动物均处死进行肺损伤组织病理学检查,并采集血样进行生化分析。血浆丙二醛(MDA)、乳酸(LA)、c反应蛋白(CRP)、白细胞介素-6 (IL-6)、肿瘤坏死因子α (TNF-α)、白细胞介素1-β (IL 1-β)水平在安慰剂组(FIP +生理盐水)和未治疗组(FIP)中显著升高,所有生物标志物的血浆水平均被催产素逆转。此外,与安慰剂组相比,催产素治疗组CT图像上肺实质密度(Hounsfield单位)和肺组织病理学损伤评分值更接近对照组。提示催产素对fip诱导的ARDS具有抗炎、抗氧化和保护作用。
Protective effect of oxytocin through its anti-inflammatory and antioxidant role in a model of sepsis-induced acute lung injury: Demonstrated by CT and histological findings.
Although several studies demonstrate the anti-inflammatory effect of oxytocin in different pathophysiological processes, there are limited data describing the impact of oxytocin on acute respiratory distress syndrome (ARDS). We aimed to elucidate the protective effect of oxytocin in ARDS with histopathological evaluation and radiological imaging in addition to biochemical markers.
Fecal intraperitoneal injection procedure (FIP) was performed on 24 of 32 rats included in the study for creating a sepsis model. Rats were randomly assigned into four groups: control group (no procedure was applied, n = 8), untreated septic group [was operated (FIP) and received no treatment, n = 8], placebo group (FIP, treated with 10 ml/kg of saline at once, n = 8), and treated group (FIP, treated with 0.1 mg/kg of oxytocin at once, n = 8). Chest CT was performed for all rats 20 hours after the procedure and density of the lungs were measured manually by using HU. All animals were sacrificed for histopathological examination of lung damage and blood samples were collected for biochemical analysis.
Plasma malondialdehyde (MDA), lactic acid (LA), C-reactive protein (CRP), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), interleukin 1-beta (IL 1-β) levels were significantly increased in the placebo (FIP + saline) and the untreated (FIP) groups, and plasma levels of all biomarkers were reversed by oxytocin. Further, the density of the lung parenchyma (Hounsfield unit) on CT images and the histopathological lung damage score values were closer to the control group in the oxytocin-treated group compared to the placebo group.
Our findings suggested that oxytocin could exert anti-inflammatory, antioxidant and protective effects in FIP-induced ARDS.
期刊介绍:
Experimental Lung Research publishes original articles in all fields of respiratory tract anatomy, biology, developmental biology, toxicology, and pathology. Emphasis is placed on investigations concerned with molecular, biochemical, and cellular mechanisms of normal function, pathogenesis, and responses to injury. The journal publishes reports on important methodological advances on new experimental modes. Also published are invited reviews on important and timely research advances, as well as proceedings of specialized symposia.
Authors can choose to publish gold open access in this journal.