Long non-coding RNA NKILA weakens TNF-alpha-induced inflammation of MRC-5 cells by miR-21 up-regulation

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-kappa B and JNK pathway-related factors (t-I kappa B alpha, p-I kappa B alpha, t-p65, p-p65, beta-actin, t-JNK and p-JNK) were tested by western blot. Otherwise, productions of inflammatory factors interleukin (IL)-1 beta 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-alpha (TNF-alpha) treatment reduced cell viability, induced cell apoptosis and promoted inflammatory factors expression. NKILA overexpression remitted TNF-alpha-induced injury. Moreover, NKILA positively regulated miR-21. miR-21 inhibition could weaken the functions of NKILA overexpression on TNF-alpha-induced injury. At last, NKILA and miR-21 were involved in the regulation of JNK and NF-kappa B pathways. Conclusions: NKILA overexpression remitted TNF-alpha-induced MRC5 cell injury by up-regulation of miR-21 and via inactivation of JNK and NF-kappa B signaling pathways.