Background::MicroRNAs are closely associated with the progression and outcomes of multiple human diseases, including sepsis. In this study, we examined the role of miR-23a in septic injury.Methods:Lipopolysaccharide (LPS) was used to induce sepsis in a rat model and H9C2 and HK-2 cells. miR-23a expression was evaluated in rat myocardial and kidney tissues, as well as H9C2 and HK-2 cells. A miR-23a mimic was introduced into cells to identify the role of miR-23a in cell viability, apoptosis, and the secretion of inflammatory cytokines. Furthermore, the effect of Rho-associated kinase 1 (n ROCK1), a miR-23a target, on cell damage was evaluated, and molecules involved in the underlying mechanism were identified.n Results::In the rat model, miR-23a was poorly expressed in myocardial (sham n vs. sepsis 1.00 ± 0.06 n vs. 0.27 ± 0.03, n P < 0.01) and kidney tissues (sham n vs. sepsis 0.27 ± 0.03 n vs. 1.00 ± 0.06, n P < 0.01). Artificial overexpression of miR-23a resulted in increased proliferative activity (DNA replication rate: Control n vs. LPS n vs. LPS + Mock n vs. LPS + miR-23a: H9C2 cells: 34.13 ± 3.12 n vs. 12.94 ± 1.21 n vs. 13.31 ± 1.43 n vs. 22.94 ± 2.26, n P < 0.05; HK-2 cells: 15.17 ± 1.43 n vs. 34.52 ± 3.46 n vs. 35.19 ± 3.12 n vs. 19.87 ± 1.52, n P < 0.05), decreased cell apoptosis (Control n vs. LPS n vs. LPS + Mock n vs. LPS + miR-23a: H9C2 cells: 11.39 ± 1.04 n vs. 32.57 ± 2.29 n vs. 33.08 ± 3.12 n vs. 21.63 ± 2.35, n P < 0.05; HK-2 cells: 15.17 ± 1.43 n vs. 34.52 ± 3.46 n vs. 35.19 ± 3.12 n vs. 19.87 ± 1.52, n P < 0.05), and decreased production of inflammatory cytokines, including interleukin-6 (Control n vs. LPS n vs. LPS + Mock n vs. LPS + miR-23a: H9C2 cells: 59.61 ± 5.14 n vs. 113.54 ± 12.30 n vs. 116.51 ± 10.69 n vs. 87.69 ± 2.97 ng/mL; n P < 0.05, n F = 12.67, HK-2 cells: 68.12 ± 6.44 n vs. 139.65 ± 16.62 n vs. 143.51 ± 13.64 n vs. 100.82 ± 9.74 ng/mL, n P < 0.05, n F = 9.83) and tumor necrosis factor-α (Controln vs. LPS n vs. LPS + Mock n vs. LPS + miR-23a: H9C2 cells: 103.20 ± 10.31 n vs. 169.67 ± 18.84 n vs. 173.61 ± 15.91 n vs. 133.36 ± 12.32 ng/mL, n P < 0.05, n F = 12.67, HK-2 cells: 132.51 ± 13.37 n vs. 187.47 ± 16.74 n vs. 143.51 ± 13.64 n vs. 155.79 ± 15.31 ng/mL, n P < 0.05, n F = 9.83) in cells. However, n ROCK1 was identified as a miR-23a target, and further up-regulation of n ROCK1 mitigated the protective function of miR-23a in LPS-treated H9C2 and HK-2 cells. Moreover, n ROCK1 suppressed sirtuin-1 (n SIRT1) expression to promote the phosphorylation of nuclear factor-kappa B (NF-κB) p65, indicating the possible involvement of this signaling pathway in miR-23a-mediated events.n Conclusion::Our results indicate that miR-23a could suppress LPS-induced cell damage and inflammatory cytokine secretion by binding to n ROCK1, mediated through the potential participation of the n SIRT1/NF-κB signaling pathway.n “,”Background::MicroRNAs are closely associated with the progression and outcomes of multiple human diseases, including sepsis. In this study, we examined the role of miR-23a in septic injury.Methods:Lipopolysaccharide (LPS) was used to induce sepsis in a rat model and H9C2 and HK-2 cells. miR-23a expression was evaluated in rat myocardial and kidney tissues, as well as H9C2 and HK-2 cells. A miR-23a mimic was introduced into cells to identify the role of miR-23a in cell viability, apoptosis, and the secretion of inflammatory cytokines. Furthermore, the effect of Rho-associated kinase 1 (n ROCK1), a miR-23a target, on cell damage was evaluated, and molecules involved in the underlying mechanism were identified.n Results::In the rat model, miR-23a was poorly expressed in myocardial (sham n vs. sepsis 1.00 ± 0.06 n vs. 0.27 ± 0.03, n P < 0.01) and kidney tissues (sham n vs. sepsis 0.27 ± 0.03 n vs. 1.00 ± 0.06, n P < 0.01). Artificial overexpression of miR-23a resulted in increased proliferative activity (DNA replication rate: Control n vs. LPS n vs. LPS + Mock n vs. LPS + miR-23a: H9C2 cells: 34.13 ± 3.12 n vs. 12.94 ± 1.21 n vs. 13.31 ± 1.43 n vs. 22.94 ± 2.26, n P < 0.05; HK-2 cells: 15.17 ± 1.43 n vs. 34.52 ± 3.46 n vs. 35.19 ± 3.12 n vs. 19.87 ± 1.52, n P < 0.05), decreased cell apoptosis (Control n vs. LPS n vs. LPS + Mock n vs. LPS + miR-23a: H9C2 cells: 11.39 ± 1.04 n vs. 32.57 ± 2.29 n vs. 33.08 ± 3.12 n vs. 21.63 ± 2.35, n P < 0.05; HK-2 cells: 15.17 ± 1.43 n vs. 34.52 ± 3.46 n vs. 35.19 ± 3.12 n vs. 19.87 ± 1.52, n P < 0.05), and decreased production of inflammatory cytokines, including interleukin-6 (Control n vs. LPS n vs. LPS + Mock n vs. LPS + miR-23a: H9C2 cells: 59.61 ± 5.14 n vs. 113.54 ± 12.30 n vs. 116.51 ± 10.69 n vs. 87.69 ± 2.97 ng/mL; n P < 0.05, n F = 12.67, HK-2 cells: 68.12 ± 6.44 n vs. 139.65 ± 16.62 n vs. 143.51 ± 13.64 n vs. 100.82 ± 9.74 ng/mL, n P < 0.05, n F = 9.83) and tumor necrosis factor-α (Controln vs. LPS n vs. LPS + Mock n vs. LPS + miR-23a: H9C2 cells: 103.20 ± 10.31 n vs. 169.67 ± 18.84 n vs. 173.61 ± 15.91 n vs. 133.36 ± 12.32 ng/mL, n P < 0.05, n F = 12.67, HK-2 cells: 132.51 ± 13.37 n vs. 187.47 ± 16.74 n vs. 143.51 ± 13.64 n vs. 155.79 ± 15.31 ng/mL, n P < 0.05, n F = 9.83) in cells. However, n ROCK1 was identified as a miR-23a target, and further up-regulation of n ROCK1 mitigated the protective function of miR-23a in LPS-treated H9C2 and HK-2 cells. Moreover, n ROCK1 suppressed sirtuin-1 (n SIRT1) expression to promote the phosphorylation of nuclear factor-kappa B (NF-κB) p65, indicating the possible involvement of this signaling pathway in miR-23a-mediated events.n Conclusion::Our results indicate that miR-23a could suppress LPS-induced cell damage and inflammatory cytokine secretion by binding to n ROCK1, mediated through the potential participation of the n SIRT1/NF-κB signaling pathway.n