Abstract：
Infantile pneumonia (IP) is an acute lower respiratory infection that imposes a heavy burden on children\'s health. Increasing evidence has demonstrated that long non-coding RNA (lncRNA) LINC00707 participates in the regulation of the pneumonia process. Cell proliferative ability and apoptosis were measured using Cell Counting Kit-8 (CCK-8), 5-ethynyl-2\'-deoxyuridine (EdU), and flow cytometry assays. Bcl-2 related X protein (Bax), NF-kB activating protein (NKAP), p-P65, P65, p-IκBα, and IκBα protein levels were detected using western blot assay. The binding between miR-382-5p and LINC00707 or NKAP was predicted by starBase v2.0 and then verified by a dual-luciferase reporter and RNA Immunoprecipitation (RIP) assays. LINC00707 and NKAP levels were increased, and miR-382-5p was decreased in LPS-stimulated WI-38 cells. Furthermore, the silencing of LINC00707 could abrogate LPS-engendered WI-38 cell proliferation, apoptosis, and oxidative stress. LINC00707 deficiency could relieve LPS-triggered WI-38 cell damage by regulating the miR-382-5p/NKAP axis, providing a new therapeutic strategy for IP treatment.
摘要：
小儿肺炎是一种急性下呼吸道感染,给儿童的健康带来沉重负担。越来越多的证据表明，长链非编码RNA（lncRNA）LINC00707参与了肺炎过程的调节。使用细胞计数试剂盒-8（CCK-8）测量细胞增殖能力和凋亡，5-乙炔基-2'-脱氧尿苷（EdU），和流式细胞术测定。Bcl-2相关X蛋白(Bax),NF-kB激活蛋白(NKAP),p-P65,P65,p-IκBα,使用蛋白质印迹法检测IκBα蛋白水平。通过starBasev2.0预测miR-382-5p与LINC00707或NKAP之间的结合，然后通过双荧光素酶报告基因和RNA免疫沉淀（RIP）测定进行验证。LINC00707和NKAP水平增加，miR-382-5p在LPS刺激的WI-38细胞中降低。此外，沉默LINC00707可以消除LPS引起的WI-38细胞增殖，凋亡，和氧化应激。LINC00707缺乏可通过调节miR-382-5p/NKAP轴减轻LPS引发的WI-38细胞损伤,为IP治疗提供新的治疗策略。
