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目的:探讨过表达长链非编码RNA（lncRNA）FAM224B对大鼠重症肺炎肺组织的保护作用及机制。方法:研究时间为2020年8月至2021年3月，将20只大鼠采用随机数字表法分为肺炎组（重症肺炎模型）和FAM224B组（重症肺炎模型+FAM224B质粒），每组10只。实时定量聚合酶链式反应（qRT-PCR）测定肺组织FAM224B水平，酶联免疫吸附测定法（ELISA）检测肺组织匀浆中肿瘤坏死因子α（TNF-α）、白细胞介素（IL）6、IL-1β水平，生物信息学软件starBase v2预测FAM224B的靶基因，qRT-PCR检测肺组织靶基因的表达，Western blot检测肺组织核因子-κB（NF-κB）信号通路蛋白表达。结果:肺炎组、FAM224B组肺组织中FAM224B表达分别为（1.09±0.23）、（10.12±1.52），肺炎组FAM224B表达明显低于FAM224B组（n t=15.86，n P < 0.01）。肺炎组肺组织匀浆中TNF-α、IL-6、IL-1β分别为（41.53±2.46）μg/L、（34.01±2.53）ng/L、（20.92±1.95）μg/L，FAM224B组分别为（21.71±2.25）μg/L、（17.13±3.01）ng/L、（11.97±1.21）μg/L，两组差异均有统计学意义（n t=15.94、14.29、13.89，均n P < 0.01）。FAM224B与miR-34b-5p存在互补结合位点。与肺炎组比较，FAM224B组肺组织中miR-34b-5p表达明显降低（n t=15.55，n P < 0.01），磷酸化核因子-κB亚单位（p-p65）、磷酸化核因子κB抑制蛋白α（p-IKB-α）蛋白表达降低。n 结论:过表达FAM224B通过抑制miR-34b-5p可减轻大鼠重症肺炎肺组织的炎性反应。“,”Objective:To investigate the protective effects of overexpression of long-chain noncoding RNA FAM224B on lung tissue of rats with severe pneumonia and the underlying mechanism.Methods:From August 2020 to March 2021, we randomly allocated 20 rats into the pneumonia group (severe pneumonia modeling) and FAM224B group (severe pneumonia modeling + FAM224B plasmid), with 10 rats in each group. We performed a quantitative real-time polymerase chain reaction to detect the level of FAM224B in lung tissue and performed an enzyme-linked immunosorbent assay to detect the levels of tumor necrosis factor-alpha, interleukin-6, and interleukin-1β in lung tissue. We used the software starBase v2.0 to predict the target gene of FAM224B. We performed a quantitative real-time polymerase chain reaction to detect the expression of the target gene in lung tissue and performed a western blot assay to detect the protein expression of the nuclear factor-kappa B signal pathway in lung tissue.Results:FAM224B expression was (1.09 ± 0.23) and (10.12 ± 1.52) in the pneumonia and FAM224B groups, respectively. FAM224B expression was significantly lower in the pneumonia group compared with the FAM224B group (n t = 15.86, n P < 0.01). The levels of tumor necrosis factor-alpha, interleukin-6, and interleukin-1β were (41.53 ± 2.46) μg/L, (34.01 ± 2.53) ng/L, (20.92 ± 1.95) μg/L in the pneumonia group and they were (21.71 ± 2.25) μg/L, (17.13 ± 3.01) ng/L, (11.97 ± 1.21) μg/L in the FAM224B group. There were significant differences in the levels of tumor necrosis factor-alpha, interleukin-6, and interleukin-1β between the two groups ( n t = 15.94, 14.29, 13.89, all n P < 0.01). FAM224B had complementary binding sites with miR-34b-5p. The expression level of miR-34b-5p in lung tissue was significantly lower in the FAM224B group compared with the pneumonia group ( n t = 15.55, n P < 0.01). The protein expression levels of phosphorylated nuclear factor-κB subunit (p-p65) and phosphorylated inhibitor of kappa B alpha in lung tissue were significantly lower in the FAM224B group compared with the pneumonia group.n Conclusion:FAM224B overexpression reduces the inflammatory reaction in lung tissue of rats with severe pneumonia through inhibiting miR-34b-5p expression.