Pan Wei, Xu Xiaoheng, Wang Yan, Song Xingyu
Department of Pediatrics, The Second Hospital of Jilin University, Changchun, Jilin 130041, P.R. China.
Experimental Center, Jilin Police College, Changchun, Jilin 130117, P.R. China.
Exp Ther Med. 2020 Mar;19(3):1695-1700. doi: 10.3892/etm.2020.8407. Epub 2020 Jan 2.
Acute lung injury (ALI) in children is a complex disease that is accompanied by an inflammatory response. The pathogenesis of ALI in children is not yet well understood. Mice with ALI exhibit inflammation of the lungs and decreased expression of interleukin (IL)-35. To investigate whether the function of IL-35 affects lipopolysaccharide (LPS)-induced ALI, IL-35 was overexpressed in cells. Enzyme-linked immunosorbent assays indicated decreased levels of IL-6 and tumor necrosis factor-α in LPS-induced and agomir-IL-35-treated murine RAW264.7 macrophages. Finally, toll-like receptor 4 (TLR4)/NF-κB signaling pathways were analyzed. The expression of TLR4, NF-κB p65 and NF-κB p50 were decreased, as was the degradation of NF-κB inhibitor-α, in LPS-induced and agomir-IL-35-treated murine RAW264.7 macrophages. The results of the present study demonstrated that IL-35 may exhibit a protective role in ALI by modulating the TLR4/NF-κB signaling pathways.
儿童急性肺损伤（ALI）是一种伴有炎症反应的复杂疾病。儿童ALI的发病机制尚未完全明确。患有ALI的小鼠表现出肺部炎症以及白细胞介素（IL）-35表达降低。为了研究IL-35的功能是否影响脂多糖（LPS）诱导的ALI，在细胞中过表达了IL-35。酶联免疫吸附测定表明，在LPS诱导且经agomir-IL-35处理的小鼠RAW264.7巨噬细胞中，IL-6和肿瘤坏死因子-α水平降低。最后，分析了Toll样受体4（TLR4）/核因子κB（NF-κB）信号通路。在LPS诱导且经agomir-IL-35处理的小鼠RAW264.7巨噬细胞中，TLR4、NF-κB p65和NF-κB p50的表达降低，NF-κB抑制剂-α的降解也减少。本研究结果表明，IL-35可能通过调节TLR4/NF-κB信号通路在ALI中发挥保护作用。
