Circular RNA (circRNA) represents an important regulator in infantile pneumonia progression. To clarify the role of circ_0026579 in this disease, LPS was used to treat WI-38 cells to mimic inflammation injury. The levels of inflammatory factors were determined by ELISA assay. Cell proliferation and apoptosis were measured by MTT assay, EdU staining and flow cytometry. The protein levels of cyclinD1, cleaved-caspase-3 and insulin-like growth factor 2 (IGF2) were examined using Western blot analysis. Cell oxidative stress was assessed by detecting MDA level and SOD activity. The expression of circ_0026579, miR-24-3p and IGF2 were analyzed using quantitative real-time PCR, and the interaction between miR-24-3p and circ_0026579 or IGF2 was confirmed by dual-luciferase reporter assay and RIP assay. LPS induced inflammation in WI-38 cells. Circ_0026579 expression was promoted in LPS-induced WI-38 cells, and its knockdown alleviated LPS-induced WI-38 cells inflammation. MiR-24-3p was sponged by circ_0026579, and its expression was reduced by LPS. MiR-24-3p inhibitor reversed the regulation of circ_0026579 knockdown on LPS-induced WI-38 cells inflammation. IGF2 was targeted by miR-24-3p, and its expression could be enhanced by LPS. MiR-24-3p relieved the inflammation of WI-38 cells which could be abolished by IGF2 overexpression. Circ_0026579 positively regulated IGF2 expression through sponging miR-24-3p. Circ_0026579 knockdown alleviated LPS-induced WI-38 cells inflammation by miR-24-3p/IGF2 axis, suggesting that circ_0026579 might contribute to infantile pneumonia progression.

环状 RNA (circRNA) 是婴儿肺炎进展的重要调节因子。为了阐明 circ_0026579 在这种疾病中的作用，LPS 被用来治疗 WI-38 细胞以模拟炎症损伤。ELISA法测定炎症因子水平。通过MTT法、EdU染色和流式细胞术测量细胞增殖和凋亡。使用蛋白质印迹分析检测 cyclinD1、cleaved-caspase-3 和胰岛素样生长因子 2 (IGF2) 的蛋白质水平。通过检测 MDA 水平和 SOD 活性来评估细胞氧化应激。使用定量实时PCR分析circ_0026579、miR-24-3p和IGF2的表达，并通过双荧光素酶报告基因测定和RIP测定证实miR-24-3p与circ_0026579或IGF2之间的相互作用。LPS 在 WI-38 细胞中诱导炎症。Circ_0026579 在 LPS 诱导的 WI-38 细胞中的表达得到促进，其敲低可减轻 LPS 诱导的 WI-38 细胞炎症。MiR-24-3p 被 circ_0026579 吸收，LPS 降低了其表达。MiR-24-3p 抑制剂逆转了 circ_0026579 敲低对 LPS 诱导的 WI-38 细胞炎症的调节。IGF2被miR-24-3p靶向，LPS可以增强其表达。MiR-24-3p 减轻了 WI-38 细胞的炎症，而 IGF2 过表达可以消除这种炎症。Circ_0026579 通过海绵化 miR-24-3p 正向调节 IGF2 表达。Circ_0026579 敲低通过 miR-24-3p/IGF2 轴减轻 LPS 诱导的 WI-38 细胞炎症，这表明 circ_0026579 可能有助于婴儿肺炎的进展。其敲低减轻了 LPS 诱导的 WI-38 细胞炎症。MiR-24-3p 被 circ_0026579 吸收，LPS 降低了其表达。MiR-24-3p 抑制剂逆转了 circ_0026579 敲低对 LPS 诱导的 WI-38 细胞炎症的调节。IGF2被miR-24-3p靶向，LPS可以增强其表达。MiR-24-3p 减轻了 WI-38 细胞的炎症，而 IGF2 过表达可以消除这种炎症。Circ_0026579 通过海绵化 miR-24-3p 正向调节 IGF2 表达。Circ_0026579 敲低通过 miR-24-3p/IGF2 轴减轻 LPS 诱导的 WI-38 细胞炎症，这表明 circ_0026579 可能有助于婴儿肺炎的进展。其敲低减轻了 LPS 诱导的 WI-38 细胞炎症。MiR-24-3p 被 circ_0026579 吸收，LPS 降低了其表达。MiR-24-3p 抑制剂逆转了 circ_0026579 敲低对 LPS 诱导的 WI-38 细胞炎症的调节。IGF2被miR-24-3p靶向，LPS可以增强其表达。MiR-24-3p 减轻了 WI-38 细胞的炎症，而 IGF2 过表达可以消除这种炎症。Circ_0026579 通过海绵化 miR-24-3p 正向调节 IGF2 表达。Circ_0026579 敲低通过 miR-24-3p/IGF2 轴减轻 LPS 诱导的 WI-38 细胞炎症，这表明 circ_0026579 可能有助于婴儿肺炎的进展。MiR-24-3p 抑制剂逆转了 circ_0026579 敲低对 LPS 诱导的 WI-38 细胞炎症的调节。IGF2被miR-24-3p靶向，LPS可以增强其表达。MiR-24-3p 减轻了 WI-38 细胞的炎症，而 IGF2 过表达可以消除这种炎症。Circ_0026579 通过海绵化 miR-24-3p 正向调节 IGF2 表达。Circ_0026579 敲低通过 miR-24-3p/IGF2 轴减轻 LPS 诱导的 WI-38 细胞炎症，这表明 circ_0026579 可能有助于婴儿肺炎的进展。MiR-24-3p 抑制剂逆转了 circ_0026579 敲低对 LPS 诱导的 WI-38 细胞炎症的调节。IGF2被miR-24-3p靶向，LPS可以增强其表达。MiR-24-3p 减轻了 WI-38 细胞的炎症，而 IGF2 过表达可以消除这种炎症。Circ_0026579 通过海绵化 miR-24-3p 正向调节 IGF2 表达。Circ_0026579 敲低通过 miR-24-3p/IGF2 轴减轻 LPS 诱导的 WI-38 细胞炎症，这表明 circ_0026579 可能有助于婴儿肺炎的进展。