Background: Infantile pneumonia (IP) seriously affects the health of children. This article mainly discussed the protective effect of long non-coding RNA NKILA (lnc NKILA) on IP by detecting cell viability, apoptosis and inflammatory response of MRC5 cells. Methods: Cell counting kit-8 (CCK-8) was used to detect cell viability, while flow cytometry was used to detect cell apoptosis. The expression of apoptosis-associated factors (Bcl-2, Bax, PARP and Cleaved-PARP) and NF-jB and JNK pathway-related factors (t-IjBa, p-IjBa, t-p65, p-p65, b-actin, t-JNK and p-JNK) were tested by western blot. Otherwise, productions of inflammatory factors interleukin (IL)-1b and IL-6 were tested by enzyme-linked immunosorbent assay (ELISA) and western blot. Furthermore, RNA levels were respectively tested and changed by RT-qPCR and cell transfection. Results: Tumour necrosis factor-a (TNF-a) treatment reduced cell viability, induced cell apoptosis and promoted inflammatory factors expression. NKILA overexpression remitted TNF-a-induced injury. Moreover, NKILA positively regulated miR-21. miR-21 inhibition could weaken the functions of NKILA overexpression on TNF-a-induced injury. At last, NKILA and miR-21 were involved in the regulation of JNK and NF-jB pathways. Conclusions: NKILA overexpression remitted TNF-a-induced MRC5 cell injury by up-regulation of miR-21 and via inactivation of JNK and NF-jB signaling pathways.
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