Peroxiredoxin 6 mediates the protective function of curcumin pretreatment in acute lung injury induced by serum from patients undergoing one-lung ventilation in vitro

Abstract

Background Curcumin has attracted much attention due to its wide range of therapeutic effects. In this study, we used serum collected from patients undergoing one-lung ventilation (OLV) to establish an in vitro acute lung injury (ALI) model to explore the potential protective mechanism of curcumin on ALI. Our study provides a new reference for the prevention and treatment of ALI induced by OLV. Methods A549 cells were treated with 20% serum from patients undergoing OLV to establish an in vitro ALI model. Curcumin, at a dose of 40 μg/ml, was administered two hours prior to this model. The levels of inflammation and oxidative stress markers were observed by Western blot, qRT–PCR, ELISA and reactive oxygen species assay. Additionally, the expression of peroxiredoxin 6 (Prdx6) and proteins involved in the NF-κB signaling pathway was evaluated. Results Twenty percent of serum collected from patients undergoing OLV downregulated the expression of Prdx6, leading to the activation of the NF-κB signaling pathway, which was associated with the subsequent overproduction of inflammatory cytokines and reactive oxygen species. Pretreatment with curcumin restored Prdx6 downregulation and inhibited NF-κB pathway activation by suppressing the nuclear translocation of P65, eventually reducing inflammation and oxidative stress damage in A549 cells. Conclusions Prdx6 mediated the protective function of curcumin by inhibiting the activation of the NF-κB pathway in ALI in vitro.

Double edged roles of endogenous PRDX6 in ventilator-induced lung injury via modulating oxidative stress and macrophages activation

“…It plays a crucial role in maintaining redox balance of lung tissue, repairing membrane damages caused by oxidative stress, and participating in the regulation of lung in ammation and injury [9,10]. A recent report has suggested that phospholipase activity of PRDX6 might mediates VILI pathogenesis [11]. However, PRDX6 is a dual-enzyme protein, and its overall changes and phospholipase role in mechanical ventilator-related in ammation have not been clearly investigated, which raises our concerns.…”

Transcutaneous electrical acupoint stimulation improves pulmonary function by regulating oxidative stress during one-lung ventilation in patients with lung cancer undergoing thoracoscopic surgery: a randomized controlled trial

“…One-lung ventilation (OLV) has allowed increasingly complex thoracic surgery and is a de facto indispensability with the increased use of minimally invasive techniques. Nevertheless, as a kind of nonphysiological ventilation mode, OLV has been viewed as a risk factor for acute lung injury (ALI) and is known to be associated with postoperative pulmonary complications [1]. Moreover, the nondependent lung is reventilated and reoxygenated after the restoration of two-lung ventilation, which leads to hypoxia-reoxygenation injury similar to ischemia-reperfusion injury with an increase in malondialdehyde (MDA) levels and reactive oxygen species (ROS) production [2].…”