SNHG16 silencing reversed LPS-induced pyroptosis in BEAS-2B cells via miR-339-5p/NLRP1 axis mediation. Our study might shed new light on exploring therapeutic strategies for the treatment of septic lung injury.

To mimic septic lung injury in vitro, cells were treated with 1 µg/ml LPS. The Cell Counting Kit-8 (CCK-8) assay was performed to test cell viability. The lactate dehydrogenase (LDH) level was detected using a commercial kit. Interleukin (IL)-18 and IL-1 β secretion was tested using ELISA. Pyroptosis was investigated via flow cytometry. The relationship among SNHG16, miR-339-5p, and NLR family pyrin domain containing 1 (NLRP1) was explored using the dual luciferase assay.

To mimic septic lung injury in vitro, cells were treated with 1 µg/ml LPS. The Cell Counting Kit-8 (CCK-8) assay was performed to test cell viability. The lactate dehydrogenase (LDH) level was detected using a commercial kit. Interleukin (IL)-18 and IL-1 β secretion was tested using ELISA. Pyroptosis was investigated via flow cytometry. The relationship among SNHG16, miR-339-5p, and NLR family pyrin domain containing 1 (NLRP1) was explored using the dual luciferase assay.

LPS significantly upregulated the levels of SNHG16 and NLRP1 in BEAS-2B cells. In addition, LPS significantly induced pyroptosis in BEAS2B cells, while this phenomenon was reversed by SNHG16 silencing. SNHG16 could bind with miR-339-5p, and NLRP1 was found to be the downstream mRNA of miR-339-5p. SNHG16 silencing significantly abolished the LPS-induced upregulation of NLRP1 through miR-339-5p downregulation. The upregulation of miR-339-5p inhibited the pro-apoptotic effect of LPS on BEAS-2B cells, which was abolished by NLRP1 overexpression. Furthermore, the anti-pyroptotic effect of SNHG16 siRNA was abolished by NLRP1 upregulation. Conclusions: SNHG16 silencing reversed LPS-induced pyroptosis in BEAS-2B cells via miR-339-5p/NLRP1 axis mediation. Our study might shed new light on exploring therapeutic strategies for the treatment of septic lung injury.