Linoleic Acid Promotes Mitochondrial Biogenesis and Alleviates Acute Lung Injury

IF 1.9 4区 医学 Q3 RESPIRATORY SYSTEM Clinical Respiratory Journal Pub Date : 2024-09-23 DOI:10.1111/crj.70004
Jie Liu, Yu Jiang, Qiuhong Zhang, Yin Qin, Kexin Li, Yu Xie, Tingting Zhang, Xiaoliang Wang, Xi Yang, Li Zhang, Gang Liu
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Abstract

Introduction

Acute lung injury (ALI) is a critical and lethal medical condition. This syndrome is characterized by an imbalance in the body's oxidation stress and inflammation. Linoleic acid (LA), a polyunsaturated fatty acid, has been extensively studied for its potential health benefits, including anti-inflammatory and antioxidant activities. However, the therapeutic effects of LA on ALI remain unexplored.

Methods

Lipopolysaccharide (LPS), found in gram-negative bacteria's outer membrane, was intraperitoneally injected to induce ALI in mice. In vitro model was established by LPS stimulation of mouse lung epithelial 12 (MLE-12) cells.

Results

LA treatment demonstrated a significant amelioration in LPS-induced hypothermia, poor state, and pulmonary injury in mice. LA treatment resulted in a reduction in the concentration of bronchoalveolar lavage fluid (BALF) protein and an increase in myeloperoxidase (MPO) activity in LPS-induced mice. LA treatment reduced the generation of white blood cells. LA treatment reduced cell-free (cfDNA) release and promote adenosine triphosphate (ATP) production. LA increased the levels of superoxide dismutase (SOD) and glutathione (GSH) but decreased the production of malondialdehyde (MDA). LA treatment enhanced mitochondrial membrane potential. LA attenuated LPS-induced elevations of inflammatory cytokines in both mice and cells. Additionally, LA exerted its protective effect against LPS-induced damage through activation of the peroxisome proliferator-activated receptor γ coactivator l alpha (PGC-1α)/nuclear respiratory factor 1 (NRF1)/transcription factor A of the mitochondrion (TFAM) pathway.

Conclusion

LA may reduce inflammation and stimulate mitochondrial biogenesis in ALI mice and MLE-12 cells.

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亚油酸促进线粒体生物生成并缓解急性肺损伤
简介急性肺损伤(ALI)是一种严重的致命性疾病。这种综合征的特点是体内氧化压力和炎症失衡。亚油酸(LA)是一种多不饱和脂肪酸,因其潜在的健康益处,包括抗炎和抗氧化活性,已被广泛研究。然而,亚油酸对 ALI 的治疗效果仍有待探索:方法:腹腔注射革兰氏阴性细菌外膜中的脂多糖(LPS)诱发小鼠 ALI。通过 LPS 刺激小鼠肺上皮细胞 12(MLE-12)建立体外模型:结果:LA治疗明显改善了LPS诱导的小鼠低体温、不良状态和肺损伤。在 LPS 诱导的小鼠中,LA 治疗导致支气管肺泡灌洗液(BALF)蛋白浓度降低,髓过氧化物酶(MPO)活性升高。LA 治疗减少了白细胞的生成。LA 可减少细胞游离 DNA(cfDNA)的释放,促进三磷酸腺苷(ATP)的产生。LA 增加了超氧化物歧化酶(SOD)和谷胱甘肽(GSH)的水平,但减少了丙二醛(MDA)的产生。LA 可增强线粒体膜电位。LA 可减轻 LPS 诱导的小鼠和细胞炎症细胞因子的升高。此外,LA 通过激活过氧化物酶体增殖激活受体 γ 辅激活因子 l alpha(PGC-1α)/核呼吸因子 1(NRF1)/线粒体转录因子 A(TFAM)途径,对 LPS 诱导的损伤发挥保护作用:LA可减轻ALI小鼠和MLE-12细胞的炎症反应并刺激线粒体的生物生成。
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来源期刊
Clinical Respiratory Journal
Clinical Respiratory Journal 医学-呼吸系统
CiteScore
3.70
自引率
0.00%
发文量
104
审稿时长
>12 weeks
期刊介绍: Overview Effective with the 2016 volume, this journal will be published in an online-only format. Aims and Scope The Clinical Respiratory Journal (CRJ) provides a forum for clinical research in all areas of respiratory medicine from clinical lung disease to basic research relevant to the clinic. We publish original research, review articles, case studies, editorials and book reviews in all areas of clinical lung disease including: Asthma Allergy COPD Non-invasive ventilation Sleep related breathing disorders Interstitial lung diseases Lung cancer Clinical genetics Rhinitis Airway and lung infection Epidemiology Pediatrics CRJ provides a fast-track service for selected Phase II and Phase III trial studies. Keywords Clinical Respiratory Journal, respiratory, pulmonary, medicine, clinical, lung disease, Abstracting and Indexing Information Academic Search (EBSCO Publishing) Academic Search Alumni Edition (EBSCO Publishing) Embase (Elsevier) Health & Medical Collection (ProQuest) Health Research Premium Collection (ProQuest) HEED: Health Economic Evaluations Database (Wiley-Blackwell) Hospital Premium Collection (ProQuest) Journal Citation Reports/Science Edition (Clarivate Analytics) MEDLINE/PubMed (NLM) ProQuest Central (ProQuest) Science Citation Index Expanded (Clarivate Analytics) SCOPUS (Elsevier)
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