Background Asthma is a chronic disease affecting the lower respiratory tract, which can lead to death in severe cases. The cause of asthma is not fully known, so exploring its potential mechanism is necessary for the targeted therapy of asthma. Method Asthma mouse model was established with ovalbumin (OVA). H&E staining, immunohistochemistry and ELISA were used to detect the inflammatory response in asthma. Transcriptome sequencing was performed to screen differentially expressed genes (DEGs). The role of KIF23 silencing in cell viability, proliferation and apoptosis was explored by cell counting kit-8, EdU assay and flow cytometry. Effects of KIF23 knockdown on inflammation, oxidative stress and pyroptosis were detected by ELISA and western blot. After screening KIF23-related signalling pathways, the effect of KIF23 on p53 signalling pathway was explored by western blot. Results In the asthma model, the levels of caspase-3, IgG in serum and inflammatory factors (interleukin (IL)-1β, KC and tumour necrosis factor (TNF)-α) in serum and bronchoalveolar lavage fluid were increased. Transcriptome sequencing showed that there were 352 DEGs in the asthma model, and 7 hub genes including KIF23 were identified. Knockdown of KIF23 increased cell proliferation and inhibited apoptosis, inflammation and pyroptosis of BEAS-2B cells induced by IL-13 in vitro. In vivo experiments verified that knockdown of KIF23 inhibited oxidative stress, inflammation and pyroptosis to alleviate OVA-induced asthma mice. In addition, p53 signalling pathway was suppressed by KIF23 knockdown. Conclusion Knockdown of KIF23 alleviated the progression of asthma by suppressing pyroptosis and inhibited p53 signalling pathway. Data are available in a public, open access repository. The datasets used and/or analysed during the current study have been uploaded to NCBI SRA database ().

中文翻译：

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KIF23 的敲低通过抑制焦亡来缓解哮喘的进展

背景 哮喘是一种影响下呼吸道的慢性疾病，严重时可导致死亡。哮喘的病因尚不完全清楚，因此探索其潜在机制对于哮喘的靶向治疗是必要的。方法用卵清蛋白（OVA）建立哮喘小鼠模型。采用H&E染色、免疫组化和ELISA检测哮喘炎症反应。进行转录组测序以筛选差异表达基因（DEG）。通过细胞计数试剂盒-8、EdU 测定和流式细胞术探讨 KIF23 沉默在细胞活力、增殖和凋亡中的作用。通过 ELISA 和蛋白质印迹检测 KIF23 敲低对炎症、氧化应激和细胞焦亡的影响。筛选KIF23相关信号通路后，通过western blot探讨KIF23对p53信号通路的影响。结果 哮喘模型中血清中caspase-3、IgG以及血清和支气管肺泡灌洗液中炎症因子（白细胞介素（IL）-1β、KC、肿瘤坏死因子（TNF）-α）水平升高。转录组测序显示哮喘模型中有352个DEG，并鉴定出包括KIF23在内的7个枢纽基因。 KIF23 的敲低可增加细胞增殖并抑制 IL-13 体外诱导的 BEAS-2B 细胞凋亡、炎症和细胞焦亡。体内实验证实，敲低 KIF23 可以抑制氧化应激、炎症和细胞焦亡，从而缓解 OVA 诱导的小鼠哮喘。此外，p53信号通路被KIF23敲低所抑制。结论 敲低KIF23通过抑制细胞焦亡和抑制p53信号通路来减轻哮喘的进展。数据可在公共、开放访问存储库中获取。当前研究期间使用和/或分析的数据集已上传至 NCBI SRA 数据库（）。