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Role and Mechanism of Maresin-1 in Acute Lung Injury Induced by Trauma-Hemorrhagic Shock

Huayi Ma, Song Mo, Qushen Yi, Junhua Lai, Huan Liu, Zhanying Shi

Department of Intensive Care Unit, The Fourth Affiliated Hospital of Guangxi Medical University, Liuzhou, Guangxi, China (mainland)

Med Sci Monit 2020; 26:e923518

DOI: 10.12659/MSM.923518

Available online: 2020-06-08

Published: 2020-08-04


BACKGROUND: It is reported that trauma hemorrhagic shock (THS) could resulted in organ injury and is related to a high mortality rate. Maresin-1 (MaR1), a derived medium through biosynthesis, is involved in inflammatory responses. However, the mechanism of MaR1 against acute lung injury needs to be further understood. This report aimed to explore whether MaR1 had a protective effect on lung injury.
MATERIAL AND METHODS: We constructed a THS-induced acute lung damage rat model and then treated the rats with MaR1. We determined Evan’s blue dye (EBD) lung permeability, lung permeability index, wet/dry (W/D) weight ratio, nitric oxide (NO) concentration and inducible nitric oxide synthase (iNOS) expression in lung tissue samples. The inflammation-related cytokines levels in the bronchoalveolar lavage fluid (BALF) and serum of rats were determined by enzyme-linked immunosorbent assay (ELISA). Finally, the TLR4/p38MAPK/NF-kappaB pathway was analyzed by quantitative real-time polymerase chain reaction and western blot assay.
RESULTS: The increased EBD ratio, lung permeability index and W/D weight ratio, NO concentration and iNOS levels were suppressed by MaR1 treatment. THS-induced over-production of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) in BALF and serum was suppressed by MaR1. Besides, the TLR4/p38MAPK/NF-kappaB pathway activation in THS-induced rats were inhibited by MaR1 treatment.
CONCLUSIONS: Our study showed that MaR1 could effectively alleviated THS-induced lung injury via inhibiting the excitation of the TLR4/p38MAPK/NF-kappaB pathway in THS-induced rats, suggesting that MaR1 might be a novel agent for lung damage treatment.

Keywords: acute lung injury, Inflammation, Mitogen-Activated Protein Kinase Kinases, NF-kappa B, Toll-Like Receptor 4



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