Methylprednisolone alleviates LPS-induced acute lung injury by inhibiting STAT3-ERK1/2 signaling pathway

Q4 Nursing

中华急诊医学杂志 Pub Date : 2019-10-09 DOI:10.3760/CMA.J.ISSN.1671-0282.2019.10.017

宋佳, S. Jia, 王春霞, W. Chunxia, 熊熙, X. Xi, 任玉倩, R. Yuqian, 张育才, Z. Yucai

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Abstract

Objective To investigate the effects of methylprednisolone on STAT3-ERK1/2 signaling pathway in lipopolysaccharide (LPS)-induced acute lung injury (ALI). Methods The C57BL/6J male mice (8-week-old) were randomly(random number) divided into 4 groups: control group (control), LPS-induced endotoxemia model (LPS), only methylprednisolone (MP) administration group (MP), and intervention group with 2 mg/kg MP (LPS+MP) (n= 8 per group). The wet/dry (W/D) weight ratio of lung tissue, lung pathology by hematoxylin & eosin (HE) staining, serum and mRNA levels of TNF-α and IL-6 in lungs were determined. The protein levels of p-STAT3 and p-ERK1/2 in lungs were detected by Western blot. Statistical analyses were performed using One-way analysis of variance test to compare among multiple groups. Results (1)MP treatment significantly decreased the lung W/D weight ratio compared with the LPS group[(3.01±0.84) vs(3.87±0.17), P = 0.038]; (2) The histopathological lesions of the lung were improved in the LPS+MP group compared with the LPS group accompanied with reduced inflammatory cell infiltration and attenuated the alveolar wall thickening; (3) The serum levels of TNF-α and IL-6 in the LPS+MP group was significantly decreased compared with the LPS group[(3.17±1.64) pg/mL vs (6.61±1.27) pg/mL, P = 0.003; (1.42±0.35) pg/mL vs (3.80±1.35) pg/mL, P = 0.008, respectively], and the mRNA levels of TNF-α and IL-6 in the LPS+MP group were significantly lower than those of the LPS group [(5.10±0.81) vs (12.2±5.05), P = 0.03; (1.62±1.00) vs (11.12±6.56), P=0.026; respectively]; (4) MP therapy significantly inhibited P-STAT3 and P-ERK1/2 protein levels [(0.26±0.05) vs (0.86±0.06), P < 0.001, (0.24±0.02) vs (1.34±0.32), P < 0.001]. Conclusions Methylprednisolone protects LPS-induced acute lung injury possibly via suppressing STAT3-ERK1/2 signaling pathway and reducing TNF-α and IL-6 expression. Key words: Methylprednisolone; STAT3; ERK1/2; Lipopolysaccharide; Acute lung injury; Sepsis; TNF-α; IL-6

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甲基强的松龙通过抑制STAT3-ERK1/2信号通路减轻lps诱导的急性肺损伤

目的探讨甲基强的松龙对脂多糖（LPS）诱导的急性肺损伤（ALI）中STAT3-ERK1/2信号通路的影响。方法将C57BL/6J雄性小鼠（8周龄）随机分为4组：对照组（对照组）、内毒素血症模型（LPS）、仅给予甲基强的松龙（MP）组（MP）和给予2mg/kg MP（LPS+MP）干预组（每组n=8）。测定肺组织的湿/干（W/D）重量比、苏木精-伊红（HE）染色的肺病理、血清和肺中TNF-α和IL-6的mRNA水平。用蛋白质印迹法检测肺组织中p-STAT3和p-ERK1/2的蛋白水平。采用单向方差分析检验进行统计分析，以在多组之间进行比较。结果（1）与LPS组相比，MP治疗显著降低了肺W/D重量比[（3.01±0.84）vs（3.87±0.17），P=0.038]；（2）与LPS组相比，LPS+MP组的肺组织病理学病变有所改善，并伴有炎症细胞浸润减少和肺泡壁增厚减轻；（3） LPS+MP组血清TNF-α和IL-6水平与LPS组相比显著降低[分别为（3.17±1.64）pg/mLvs（6.61±1.27）pg/mL，P=0.003；（1.42±0.35）pg/mL/（3.80±1.35）pg/mL，P=0.008]，LPS+MP组TNF-α和IL-6的mRNA水平显著低于LPS组[分别为（5.10±0.81）vs（12.2±5.05），P=0.03；（1.62±1.00）vs（11.12±6.56），P=0.026]；（4） MP治疗可显著抑制P-STAT3和P-ERK1/2蛋白水平[（0.26±0.05）vs（0.86±0.06），P<0.001，（0.24±0.02）vs（1.34±0.32），P=0.001]。关键词：甲基泼尼松；STAT3；ERK1/2；脂多糖；急性肺损伤；脓毒症；TNF-α；IL-6

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来源期刊

中华急诊医学杂志 Nursing-Emergency Nursing

CiteScore

0.10

自引率

0.00%

发文量

8629

期刊介绍： Chinese Journal of Emergency Medicine is the only national journal which represents the development of emergency medicine in China. The journal is supervised by China Association of Science and Technology, sponsored by Chinese Medical Association, and co-sponsored by Zhejiang University. The journal publishes original research articles dealing with all aspects of clinical practice and research in emergency medicine. The columns include Pre-Hospital Rescue, Emergency Care, Trauma, Resuscitation, Poisoning, Disaster Medicine, Continuing Education, etc. It has a wide coverage in China, and builds up communication with Hong Kong, Macao, Taiwan and international emergency medicine circles.