Department of Anesthesiology, State Key Laboratory of Oncology in Southern China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou, 510060, China.
Department of Anesthesiology, The Seventh Affiliated Hospital of Sun Yat-Sen University, Shenzhen, 518107, China.
BMC Pulm Med. 2022 May 12;22(1):192. doi: 10.1186/s12890-022-01988-y.
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.
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.
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.
Prdx6 mediated the protective function of curcumin by inhibiting the activation of the NF-κB pathway in ALI in vitro.
姜黄素因其广泛的治疗效果而受到广泛关注。在这项研究中，我们使用接受单肺通气（OLV）的患者的血清建立了体外急性肺损伤（ALI）模型，以探讨姜黄素对 ALI 的潜在保护机制。我们的研究为预防和治疗 OLV 引起的 ALI 提供了新的参考。
用接受 OLV 的患者的 20%血清处理 A549 细胞，以建立体外 ALI 模型。在该模型之前两小时给予 40μg/ml 的姜黄素。通过 Western blot、qRT-PCR、ELISA 和活性氧测定观察炎症和氧化应激标志物的水平。此外，还评估了过氧化物酶 6（Prdx6）和参与 NF-κB 信号通路的蛋白质的表达。
接受 OLV 的患者的 20%血清下调了 Prdx6 的表达，导致 NF-κB 信号通路的激活，这与随后的炎症细胞因子和活性氧的过度产生有关。姜黄素预处理通过抑制 P65 的核易位，恢复 Prdx6 的下调并抑制 NF-κB 通路的激活，最终减少 A549 细胞中的炎症和氧化应激损伤。
Prdx6 通过抑制 NF-κB 通路的激活介导了姜黄素在体外 ALI 中的保护作用。
