Cui Pei, Feng Xiaoyan, Zhu Feng, Yao Yongming, Xiao Shichu, Gong Zhenyu, Xin Haiming, Zhan Qiu, Yang Fuwang, Deng Chunjiang, Tang Zhiping, Tong Yalin, Xia Zhaofan
Research Laboratory of Burns and Trauma, the 181st Hospital of Chinese PLA, Guilin, China.
Department of Burns, Plastic and Wound repair surgery, the 181st Hospital of Chinese PLA, Guilin, China.
Cell Physiol Biochem. 2018;47(6):2396-2406. doi: 10.1159/000491614. Epub 2018 Jul 10.
BACKGROUND/AIMS: White smoke inhalation (WSI) is an uncommon but potentially deadly cause of acute respiratory distress syndrome (ARDS). However, no clinical treatment protocol has been established for the treatment of WSI-induced ARDS. Therefore, it is necessary to investigate the effects of WSI in ARDS and the mechanisms underlying the effects of WSI to determine a novel therapeutic target.
On the basis of the duration of continued inhalation of white smoke (3 min, 5 min, and 7 min), rats were divided into three groups (WSI-3 min, WSI-5 min, and WSI-7 min). The survival rate, pathological change, and computed tomography (CT) score were evaluated to determine the modeling conditions. In the established WSI-5 min models, evaluations were performed to evaluate the following: arterial blood gas levels, lung wet/dry weight ratio, the expression of inflammatory cytokines, and the effect of NF-κB signaling pathway.
The survival rate of rats at 72 h post-WSI in the WSI-3 min, WSI-5 min, and WSI-7 min groups was 83.33%, 75%, and 25%, respectively. Results from evaluation of H&E staining, CT scan, arterial blood gas levels, and lung wet/dry weight ratio suggest that the pathological changes in the rat in the WSI-5 min and WSI-7 min groups are very similar to those in patients with ARDS induced by WSI. Additionally, the expression of INF-γ, TGF-β1, TNF-α, and IL-1β were increased, and the NF-κB signaling pathway was activated in the WSI-5 min group.
The rat model of WSI-5 min can be used as a WSI-induced ALI model for further experiments. The NF-κB signaling pathway may be a potential therapeutic target for the treatment of WSI- induced ARDS.
背景/目的:吸入白烟(WSI)是急性呼吸窘迫综合征(ARDS)一种罕见但可能致命的病因。然而,目前尚未建立针对WSI所致ARDS的临床治疗方案。因此,有必要研究WSI在ARDS中的作用及其作用机制,以确定新的治疗靶点。
根据持续吸入白烟的时间(3分钟、5分钟和7分钟),将大鼠分为三组(WSI - 3分钟组、WSI - 5分钟组和WSI - 7分钟组)。评估生存率、病理变化和计算机断层扫描(CT)评分以确定建模条件。在已建立的WSI - 5分钟模型中,进行以下评估:动脉血气水平、肺湿/干重比、炎性细胞因子的表达以及NF - κB信号通路的作用。
WSI - 3分钟组、WSI - 5分钟组和WSI - 7分钟组大鼠在WSI后72小时的生存率分别为83.33%、75%和25%。苏木精-伊红(H&E)染色、CT扫描、动脉血气水平和肺湿/干重比的评估结果表明,WSI - 5分钟组和WSI - 7分钟组大鼠的病理变化与WSI所致ARDS患者的病理变化非常相似。此外,WSI - 5分钟组中γ干扰素(INF - γ)、转化生长因子 - β1(TGF - β1)、肿瘤坏死因子 - α(TNF - α)和白细胞介素 - 1β(IL - 1β)的表达增加,且NF - κB信号通路被激活。
WSI - 5分钟大鼠模型可作为WSI所致急性肺损伤(ALI)模型用于进一步实验。NF - κB信号通路可能是治疗WSI所致ARDS的潜在治疗靶点。