electroacupuncture (ea) has been documented as a form of therapy for chronic sinusitis (crS). The present study aimed to assess the effects of ea combined with interleukin-10 (il-10) overexpression on crS in mice, and to investigate the associated mechanisms. a mouse model of crS was established by the administration of ovalbumin (oVa), and overexpression of il-10 was induced using virus-encoded il-10. The experimental groups were as follows: i) control group; ii) oVa group; iii) oVa + ea group; iv) oVa + empty vector group; v) oVa + vector + ea group; vi) oVa + il-10 group; and vii) oVa + il-10 + ea group. Pathological changes and nasal mucus were analyzed using hematoxylin and eosin staining. interferon-γ (iFn-γ) and il-10 were detected via reverse-transcription quantitative Pcr and western blot analyses. The pseudostratified epithelium of the mucosa of the nasal sinus was impaired following the induction of crS. Treatment with ea and/or il-10 reversed the injury. combination treatment with ea and il-10 induced synergistic effects. No infiltration of inflammatory cells was observed in the submucosa following ea and il-10 treatment. compared with the control group, the expression of iFn-γ and il-10 in the oVa group was reduced. By contrast, ea or the overexpression of il-10 inhibited this reduction. Furthermore, the combined application of EA and IL-10 had a significantly more potent inhibitory effect on the reduction of iFn-γ expression, but not il-10. collectively, ea combined with il-10 induced specific effects on CRS in mice, likely through the upregulation of iFn-γ and il-10. The current study presented mechanistic implications for the application of ea as an alternative treatment for crS.

Long non-coding RNAs (LncRNAs) are vital in the treatment of laryngeal squamous cell carcinoma (LSCC). This study estimated the mechanism of lncRNA CCAT1 (CCAT1) in LSCC cells. The expression of CCAT1 in the human laryngeal mucosal epithelial cells (HLCs) and LSCC cells (Hep-2 and TU177) was detected. CCK-8 and Transwell assays were used to evaluate the cell proliferative, migrative, and invasive abilities, respectively. The subcellular localization of CCAT1 was verified by RNA-FISH and cytoplasmic isolation assays. The targeted relationship among CCAT1, miR-218-5p, and BMI1 was verified by dual-luciferase assay. Expressions of miR-218-5p and BMI1 were detected by RT-qPCR. Our results depicted that CCAT1 was highly-expressed in Hep-2 and TU177 cells. Silencing CCAT1 inhibited the proliferation, migration, and invasion of Hep-2 and TU177 cells. Mechanically, CCAT1 regulated the BMI1 expression by competitively binding to miR-218-5p as a competing endogenous RNA (ceRNA), and thus facilitated the growth of Hep-2 and TU177 cells. Downregulation of miR-218-5p or upregulation of BMI1 inhibited the inhibitory effect of silencing CCAT1 on Hep-2 and TU177 cell proliferation, invasion, and migration. In conclusion, our study elicited that lncRNA CCAT1 facilitated the proliferation, migration, and invasion of Hep-2 and TU177 cells by sponging miR-218-5p and regulating the downstream BMI1.