Hydrogen Attenuates Endotoxin-Induced Lung Injury by Activating Thioredoxin 1 and Decreasing Tissue Factor Expression.
Hydrogen Attenuates Endotoxin-Induced Lung Injury by Activating Thioredoxin 1 and Decreasing Tissue Factor Expression.
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DOI：
10.3389/fimmu.2021.625957
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发表时间：
2021
影响因子：
7.3
通讯作者：
Liu WT
中科院分区：
文献类型：
--
作者：
Li Q;Hu L;Li J;Yu P;Hu F;Wan B;Xu M;Cheng H;Yu W;Jiang L;Shi Y;Li J;Duan M;Long Y;Liu WT
内毒素引起的肺损伤是内毒素血症引起死亡的主要原因之一，然而，有效的治疗方法很少。氢气吸入是一种有效的治疗炎症性肺损伤的方法，但其机制尚不清楚。本研究旨在探讨氢气对内毒素性肺损伤的保护作用，为氢气的临床应用提供参考。采用内毒素（LPS）建立内毒素性肺损伤小鼠模型。观察生存率及肺组织病理变化。体外培养THP-1和HUVECC细胞。硫氧还蛋白1（Trx 1）抑制剂用于评价氢的抗炎作用。氢气显著提高小鼠的存活率，减少肺水肿和出血，中性粒细胞浸润和IL-6分泌。内毒素血症小鼠肺和血清中组织因子（TF）表达和MMP-9活性降低，而Trx 1表达增加。LPS刺激的THP-1和HUVEC-C细胞在体外，并表明，氢降低TF表达和MMP-9的活性，这是由Trx 1抑制剂，PX 12废除。氢通过激活Trx 1降低TF表达和MMP-9活性减轻内毒素诱导的肺损伤氢靶向Trx 1可能是内毒素诱导的肺损伤的潜在治疗方法。
Endotoxin-induced lung injury is one of the major causes of death induced by endotoxemia, however, few effective therapeutic options exist. Hydrogen inhalation has recently been shown to be an effective treatment for inflammatory lung injury, but the underlying mechanism is unknown. In the current study we aim to investigate how hydrogen attenuates endotoxin-induced lung injury and provide reference values for the clinical application of hydrogen. LPS was used to establish an endotoxin-induced lung injury mouse model. The survival rate and pulmonary pathologic changes were evaluated. THP-1 and HUVECC cells were cultured in vitro. The thioredoxin 1 (Trx1) inhibitor was used to evaluate the anti-inflammatory effects of hydrogen. Hydrogen significantly improved the survival rate of mice, reduced pulmonary edema and hemorrhage, infiltration of neutrophils, and IL-6 secretion. Inhalation of hydrogen decreased tissue factor (TF) expression and MMP-9 activity, while Trx1 expression was increased in the lungs and serum of endotoxemia mice. LPS-stimulated THP-1 and HUVEC-C cells in vitro and showed that hydrogen decreases TF expression and MMP-9 activity, which were abolished by the Trx1 inhibitor, PX12. Hydrogen attenuates endotoxin-induced lung injury by decreasing TF expression and MMP-9 activity via activating Trx1. Targeting Trx1 by hydrogen may be a potential treatment for endotoxin-induced lung injury.
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