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- W2426474677 abstract "Objectives To explore ventilation induced cytokine production and the role of oxidant stress in lung stretch. Methods Both in vitro and in vivo models of ventilator-induces lung injury (VILI) were used. Alveolar epithelial cells were stretched in vitro to mimic the lung injury in VILI. Rats were ventilated at large tidal volume to produce ventilator-induced lung injury in vivo. A total of 23 inflammatory cytokines were screened with micro gene array in stretched alveolar epithelial cells. Cytokines found to have up-regulated in cells were measured in serum and lung tissue of rats exposed to large tidal volume ventilation. For investigating the intracellular pathway of cytokine up-regulation in VILI, exogenous TNF-α or H2O2 was added to culture media of alveolar epithelial cells. Cytokines were then measured. To explore the role of oxidant stress in VILI, N-acetylcysteine(NAC), as an anti-oxidant, was used in vitro and in vivo. Results We found that transforming growth factor-β1 (TGF-β1 and transforming growth factor-β2 (TGF-β2) were up-regulated in stretched alveolar epithelial cells and also in serum of rats with large tidal volume ventilation. Tumor necrosis factor-α (TGF-α) had no effects on TGF-β production in alveolar epithelial cells. Exogenous H2O2, as an oxidant, increased TGF-β production in alveolar epithelial cells. NAC, an anti-oxidant, decreased stretch induced TGF-β production, along with a down-regulation of oxidant injury. NAC also blocked the up-regulation of TGF-β in vivo model of VILI. Conclusion TGF-β1 and TGF-β2 were up-regulated in VILI. Oxidant injury mediated up-regulation of TGF-β in VILI. NAC, which attenuated oxidant injury and blocked TGF-β up-regulation in VILI, could be a future therapeutic strategy in VILI." @default.
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- W2426474677 date "2006-01-10" @default.
- W2426474677 modified "2023-09-27" @default.
- W2426474677 title "Oxidant injury mediates TGF-β up-regulation in ventilator induced lung injury" @default.
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