Long noncoding RNA ameliorates chronic intermittent hypoxia-induced lung inflammation by regulating axis.

Purpose: The purpose is to confirm whether long noncoding RNA relieves chronic intermittent hypoxia (CIH)-induced lung inflammation.

Methods: Male Sprague Dawley rats were used to establisha CIH rat model. Hematoxylin and Eosin staining was used on the lung tissue injury to determine the successful construction of CIH animal model. Arterial partial pressure of oxygen (PaO) and carbon dioxide (PaCO) were measured. was overexpressed to evaluate its role in the progression and development of CIH. T cell differentiation and cytokine production were determined using flow cytometry. Cell apoptosis was determined using terminal deoxynucleotidyl transferase dUTP nick end labelling assay kit. The target of and was predicted by the Encyclopedia of RNA Interactomes (ENCORI) and confirmed using luciferase assay.

Results: was downregulated in CIH rat models. Lung tissue injury was observed in CIH rats, and the injury was attenuated by the overexpression of . PaO was reduced and PaCO was induced in CIH rats, which was reversed by the overexpression of . The overexpression of inhibited CIH-induced cell apoptosis. It also reversed alterations in the levels of interferon gamma (IFNγ), interleukin (IL)-2, IL-6, IL-1β, tumor necrosis factor alpha (TNF-α), and transforming growth factor beta1 (TGF-β1) in rats caused by CIH. The overexpression of prevented the induction in CD4 IFN-γ T cells and reduction in CD4TGF-β1 T cells. The overexpression of upregulated tumor necrosis factor-alpha-induced protein 8-like 2 () key regulator through directly targeting . Further experiments proved that was the direct target of .

Conclusion: This study manifested that acted as an anti-inflammatory regulator and protected lung tissue injury from CIH in the rat model; this was mediated by upregulation of through directly targeting upregulated the expression of , providing new understanding and therapeutic target for CIH.