Abstract: Objective: To investigate the effect and mechanism of long non-coding RNA (lncRNA) SNHG16 on sepsis-induced renal cell inflammation and apoptosis.Methods: Human renal proximal tubular epithelial cells (HRPTEC) was induced by lipopolysaccharide (LPS) in vitro to construct a sepsis-like renal cell model.The cells were divided into control group and LPS group.HRPTEC in LPS group were divided into SNHG16 overexpression group (LPS+SNHG16 group), overexpression empty vector group (LPS+vector group), SNHG16 overexpression combined with miR-421 mimic group (LPS+SNHG16+miR-421 mimic group) and SNHG16 overexpression combined with mitochondrial pyruvate carrier-1 (MPC-1) small interfering RNA (siRNA) silencing group (LPS+SNHG16+si-MPC-1 group).Luciferase reporter gene detection was used to verify the binding of miR-421 sequence to SNHG16 sequence and the binding of miR-421 to MPC-1 3'-UTR.Real-time fluorescence quantitative polymerase chain reaction (RT-qPCR) was used to detect the expression levels of SNHG16 and miR-421 in HRPTEC of each group, western blotting was used to detect the expression levels of cleaved-caspase 3, Bcl-2 and MPC-1 in HRPTEC of each group, cell counting kit-8 (CCK-8) method was used to detect the proliferation rate of HRPTEC of each group and the apoptosis rate was detected by flow cytometry.The levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) in cell culture supernatant of each group were detected by enzyme-linked immunosorbent assay (ELISA).Results: Compared with the control group, the cell proliferation rate of LPS group decreased (P< 0.05), the apoptosis rate increased (P< 0.05), and the expressions of miR-421, cleaved-caspase 3 and Bcl-2 increased (all P< 0.05).However, the expressions of SNHG16 and MPC-1 in cells decreased (all P< 0.05), and the expressions of TNF-α, IL-1β and IL-6 in cell culture supernatant increased (all P< 0.05).LPS treatment combined with SNHG16 overexpression increased the cell proliferation rate (P< 0.05), decreased the apoptosis (P< 0.05), and inhibited the expressions of TNF-α, IL-1β and IL-6 in cell culture supernatant (all P< 0.05).However, the above effects of SNHG16 group were partially reversed by miR-421-mimic (P< 0.05).The above effects of LPS+SNHG16 group were partially reversed by si-MPC-1 after adding si-MPC-1 to LPS+SNHG16 (all P< 0.05).Conclusion: LncRNA SNHG16 can improve sepsis-induced renal cell inflammation and apoptosis by targeting miR-421/MPC-1 axis.