Anti-inflammatory effect of tranexamic acid against trauma-hemorrhagic shock-induced acute lung injury in rats

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  • Teng Yue
    Department of Emergency Medicine, Chinese PLA General Hospital, 28 Fuxing Road, Beijing 100853, P.R. China Department of Emergency Medicine, General Hospital of Shenyang Military Area Command, 83 Wenhua Road, Shenyang 110016, P.R. China
  • Feng Cong
    Department of Emergency Medicine, Chinese PLA General Hospital, 28 Fuxing Road, Beijing 100853, P.R. China
  • Liu Yunen
    Department of Emergency Medicine, General Hospital of Shenyang Military Area Command, 83 Wenhua Road, Shenyang 110016, P.R. China Laboratory of Rescue Center for Severe Wound and Trauma PLA, 83 Wenhua Road, Shenyang 110016, P.R. China Liaoning Key Laboratory of Severe Wound and Trauma and Organ Protection, 83 Wenhua Road, Shenyang 110016, P.R. China
  • Jin Hongxu
    Department of Emergency Medicine, General Hospital of Shenyang Military Area Command, 83 Wenhua Road, Shenyang 110016, P.R. China
  • Gao Yan
    Department of Emergency Medicine, General Hospital of Shenyang Military Area Command, 83 Wenhua Road, Shenyang 110016, P.R. China
  • Li Tanshi
    Department of Emergency Medicine, Chinese PLA General Hospital, 28 Fuxing Road, Beijing 100853, P.R. China

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<p>It has been demonstrated that tranexamic acid (TXA), a synthetic derivative of lysine, alleviates lung damage in a trauma-hemorrhagic shock (T/HS) model. Nevertheless, the mechanism of TXA against acute lung injury (ALI) has not deeply elaborated. In this study, we generated a T/HS rat model based on previous research, and TXA (50 mg/kg and 100 mg/kg) was intravenously injected into these rats prior to or post T/HS. The results revealed that the decreased survival rate and impaired lung permeability of the rats caused by T/HS were improved by TXA pretreatment or posttreatment. T/HS-triggered over-generation of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in bronchoalveolar fluid and serum was inhibited by TXA, and the enzymatic activity of myeloperoxidase (MPO) in lung tissues was suppressed by TXA as well. Furthermore, TXA treatment deactivated the poly ADP-ribose polymerase-1 (PARP1)/nuclear factor κB (NF-κB) signaling pathway in the lungs of T/HS rats, as evidenced by increased IκBα expression, and decreased cleaved PARP1, p-p65 (Ser276), p-p65 (Ser529), p-IκBα (ser32/ser36), and intercellular adhesion molecule-1. While the expression level of total p65 did not change after T/HS, its DNA binding activity was strengthened. Both TXA pretreatment and posttreatment suppressed this effect on the DNA binding activity of NF-κB. Taken together, our results reveal that administration of TXA effectively relieves T/HS-induced ALI, at least in part, by attenuating the abnormal pulmonary inflammation.</p>

収録刊行物

  • Experimental Animals

    Experimental Animals 67 (3), 313-320, 2018

    公益社団法人 日本実験動物学会

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