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<p>The objective of this study was to evaluate the protective effects and elucidate the mechanism underlying Tranexamic acid (TXA) and erythropoietin (EPO) in osteoporosis hip fracture (OHF)-induced acute lung injury (ALI). Sprague-Dawley (SD) rats were randomly divided into the control, OHF, OHF + TXA, and OHF + EPO groups. Lung tissue was analyzed at 12, 24, and 48&#xa0;h post-treatment to assess injury levels through hematoxylin and eosin (H&amp;E) staining, enzyme-linked immunosorbent assay (ELISA), and Western blot analysis. H&amp;E staining showed that TXA and EPO significantly reduced the OHF-induced lung injury. The wet/dry ratios were significantly lower in the OHF + TXA and OHF + EPO groups compared to the OHF group. We found significantly lower levels of inflammatory cytokine production levels and nuclear factor-κB (NF-κB) signaling pathway activity in the lung of the OHF + TXA group and OHF + EPO group than in the hip fracture group. Moreover, TXA and EPO treatments counteracted mitochondrial injury and type II alveolar epithelial cells (AECII) cell apoptosis in OHF rats. The treatment with TXA and EPO also exhibited inhibitory effects on the increase of ER stress-related apoptosis in lung tissue after OHF, as evidenced by reduced expression levels of glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), phosphorylated (p)-protein kinase RNA-like endoplasmic reticulum kinase (PERK), p-endoplasmic reticulum-to-nucleus signaling 1 (IRE1)α, Caspase-12, activating transcription factor 4 (ATF4), Bax and induced expression of Bcl-2. Thus, TXA and EPO may have a protective effect on OHF-induced ALI.</p>

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Tranexamic acid and erythropoietin inhibited inflammatory response and endoplasmic reticulum stress and protected rats against acute lung injury caused by osteoporotic hip fracture

  • 期刊论文

  • 发表日期：

    2025年9月30日

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  • Xi Liu,
  • Dechuan Zhang,
  • Mingjin Li,
  • Huixu Ma,
  • Jinhua Cai

摘要

The objective of this study was to evaluate the protective effects and elucidate the mechanism underlying Tranexamic acid (TXA) and erythropoietin (EPO) in osteoporosis hip fracture (OHF)-induced acute lung injury (ALI). Sprague-Dawley (SD) rats were randomly divided into the control, OHF, OHF + TXA, and OHF + EPO groups. Lung tissue was analyzed at 12, 24, and 48 h post-treatment to assess injury levels through hematoxylin and eosin (H&E) staining, enzyme-linked immunosorbent assay (ELISA), and Western blot analysis. H&E staining showed that TXA and EPO significantly reduced the OHF-induced lung injury. The wet/dry ratios were significantly lower in the OHF + TXA and OHF + EPO groups compared to the OHF group. We found significantly lower levels of inflammatory cytokine production levels and nuclear factor-κB (NF-κB) signaling pathway activity in the lung of the OHF + TXA group and OHF + EPO group than in the hip fracture group. Moreover, TXA and EPO treatments counteracted mitochondrial injury and type II alveolar epithelial cells (AECII) cell apoptosis in OHF rats. The treatment with TXA and EPO also exhibited inhibitory effects on the increase of ER stress-related apoptosis in lung tissue after OHF, as evidenced by reduced expression levels of glucose-regulated protein 78 (GRP78), C/EBP homologous protein (CHOP), phosphorylated (p)-protein kinase RNA-like endoplasmic reticulum kinase (PERK), p-endoplasmic reticulum-to-nucleus signaling 1 (IRE1)α, Caspase-12, activating transcription factor 4 (ATF4), Bax and induced expression of Bcl-2. Thus, TXA and EPO may have a protective effect on OHF-induced ALI.