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首页> 外文期刊>Experimental Animals >Anti-inflammatory effect of tranexamic acid against trauma-hemorrhagic shock-induced acute lung injury in rats
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Anti-inflammatory effect of tranexamic acid against trauma-hemorrhagic shock-induced acute lung injury in rats

机译：氨甲环酸对创伤性失血性休克所致大鼠急性肺损伤的抗炎作用

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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)uclear 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.
机译：已经证明，赖氨酸的合成衍生物氨甲环酸（TXA）在创伤性失血性休克（T / HS）模型中减轻了肺损伤。然而，TXA对抗急性肺损伤（ALI）的机制尚未深入阐述。在这项研究中，我们基于先前的研究生成了T / HS大鼠模型，并在T / HS之前或之后将TXA（50 mg / kg和100 mg / kg）静脉内注射到这些大鼠中。结果表明，TXA预处理或后处理可改善T / HS引起的大鼠存活率降低和肺通透性受损。 T / HS触发的TXA抑制支气管肺泡液和血清中白介素6（IL-6）和肿瘤坏死因子-α（TNF-α）的过度生成，并且肺组织中的髓过氧化物酶（MPO）的酶活性也被TXA压制了。此外，TXA治疗使T / HS大鼠肺中的聚ADP-核糖聚合酶-1（PARP1）/核因子κB（NF-κB）信号通路失活，这由IκBα表达增加和PARP1，p- p65（Ser276），p-p65（Ser529），p-IκBα（ser32 / ser36）和细胞间粘附分子-1。 T / HS后总p65的表达水平没有变化，但其DNA结合活性增强。 TXA预处理和后处理均抑制了这种对NF-κBDNA结合活性的作用。两者合计，我们的结果表明，TXA的施用至少可以通过减轻异常的肺部炎症来有效缓解T / HS诱导的ALI。

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