首页> 外文期刊>Journal of molecular histology >N-acetylcysteine counteracts oxidative stress and protects alveolar epithelial cells from lung contusion-induced apoptosis in rats with blunt chest trauma
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N-acetylcysteine counteracts oxidative stress and protects alveolar epithelial cells from lung contusion-induced apoptosis in rats with blunt chest trauma

机译:N-乙酰半胱氨酸可抵消氧化应激并保护肺泡上皮细胞免受钝挫伤大鼠肺挫伤所致的细胞凋亡

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The aim of this study was to investigate the protective effects of N-acetylcysteine (NAC) on peroxidative and apoptotic changes in the contused lungs of rats following blunt chest trauma. The rats were randomly divided into three groups: control, contusion, and contusion + NAC. All the rats, apart from those in the control group, performed moderate lung contusion. A daily intramuscular NAC injection (150 mg/kg) was given immediately following the blunt chest trauma and was continued for two additional days following cessation of the trauma. Samples of lung tissue were taken in order to evaluate the tissue malondialdehyde (MDA) level, histopathology, and epithelial cell apoptosis using terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay and active caspase-3 immunostaining. In addition, we immunohistochemically evaluated the expression of surfactant protein D (SP-D) in the lung tissue. The blunt chest trauma-induced lung contusion resulted in severe histopathological injury, as well as an increase in the MDA level and in the number of cells identified on TUNEL assay together with active caspase-3 positive epithelial cells, but a decrease in the number of SP-D positive alveolar type 2 (AT-2) cells. NAC treatment effectively attenuated histopathologic, peroxidative, and apoptotic changes, as well as reducing alterations in SP-D expression in the lung tissue. These findings indicate that the beneficial effects of NAC administrated following blunt chest trauma is related to the regulation of oxidative stress and apoptosis.
机译:这项研究的目的是调查N-乙酰半胱氨酸(NAC)对钝性胸外伤大鼠挫伤后肺中过氧化和凋亡变化的保护作用。将大鼠随机分为三组:对照组,挫伤和挫伤+ NAC。除对照组外,所有大鼠均表现为中度肺挫伤。钝性胸部外伤后立即进行每日肌内NAC注射(150 mg / kg),并在外伤停止后继续进行另外两天。为了评估组织丙二醛(MDA)的水平,组织病理学和上皮细胞凋亡,采用了末端脱氧核苷酸转移酶dUTP缺口末端标记(TUNEL)分析和活性caspase-3免疫染色,对肺组织进行了采样。此外,我们免疫组织化学评估了肺组织中表面活性蛋白D(SP-D)的表达。钝性胸外伤引起的肺挫伤导致严重的组织病理学损伤,以及通过TUNEL测定鉴定出的MDA水平和细胞数量与活性的caspase-3阳性上皮细胞一起增加,但减少了SP-D阳性2型肺泡(AT-2)细胞。 NAC治疗可有效减轻组织病理学,过氧化和凋亡变化,并减少肺组织中SP-D表达的变化。这些发现表明,钝性胸外伤后给予NAC的有益作用与氧化应激和细胞凋亡的调节有关。

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