Objective To investigate the role of long chain non coding ribonucleic acid (LNcRNA) small nucleolar RNA host gene 14 (SNHG14) in regulating microribonucleic acid 223-3p (miR-223-3p) in alleviating sepsis associated lung injury in rats. Methods Sepsis rat models were established and the rats were randomly divided into SNHG14 upregulation group, SNHG14 upregulated control group, SNHG14 downregulation group, SNHG14 downregulation control group, miR-223-3p upregulation group, miR-223-3p upregulation control group, miR-223-3p downregulation group, miR-223-3p downregulation control group, and model group. Sham operation group was set up simutalously. All of them were administered through the tail vein. After 48 hours, the lung tissues was euthanized to detect the expressions of LncRNA SNHG14 and miR-223-3p. Tumor necrosis factor α (TNF- α), interleukin-1β (IL-1β), interleukin-18 (IL-18), lung wet weight/dry weight ratio (W/D) and the alveolar fluid clearance rate (AFC) were detected. Pathological changes in lung tissues were observed. Human NOD like receptor family protein 3 (NLPR3), cysteine-requiring aspartate protease 1 (caspase-1), and 1-aminocyclopropane-1-carboxylate synthase (ACS) genes and proteins expressions in lung tissues were detected. The dual luciferase reporter gene experiment was used to verify the targeted regulatory effect of LncRNA SNHG14 on miR-223-3p. Results Compared with the sham operation group, the model group showed increase in lung tissue LncRNA SNHG14 expression, serum inflammatory factor levels, W/D, pathological change quantification score, and lung tissue NLPR3, caspase-1 and ACS expressions (P<0.05), decrease in miR-223-3p expression and AFC (P<0.05). Compared with the model group and corresponding control groups, the SNHG14 upregulation group showed increase in LncRNA SNHG14 expression (P<0.05), and the SNHG14 upregulation group and the miR-223-3p downregulation group showed decrease in miR-223-3p expression and AFC (P<0.05), and increase in the levels of serum inflammatory factors, W/D, quantitative scores of pathological changes, and the expressions of NLPR3, caspase-1 and ACS in lung tissues (P<0.05). Compared with the model group and corresponding control groups, the expression of LncRNA SNHG14 in the SNHG14 downregulation group decreased (P<0.05), while the expression of miR-223-3p and AFC in the SNHG14 downregulation group and miR-223-3p upregulation group increased (P<0.05), which showed decrease in the levels of serum inflammatory factors, W/D, quantitative scores of pathological changes, and the expressions of NLPR3, caspase-1 and ACS in lung tissues (P<0.05). There were binding sites between LncRNA SNHG14 and miR-223-3p, and the former could negatively feedback targeted to regulate the latter. Conclusion Downregulation of LncRNA SNHG14 targets an increase in miR-223-3p expression and inhibit the NLRP3 pathway to alleviate sepsis related lung injury, which is related to the inhibition of inflammatory response, while upregulation of LncRNA SNHG14 negatively feedback targeting miR-223-3p and activated the NLRP3 pathway to exacerbate sepsis related lung injury.