Abstract:Objective To investigate the effects and mechanism of polydatin on the lipopolysaccharide-induced mitochondrial injury in alveolar epithelial cells. Methods A549 cells were assigned to four groups. Cells in the control group were treated with 0.1% DMSO for 7h only; those in model group received the pretreatment of 0.1% DMSO for 1 h and were incubated with LPS (5mg/L) for 6h; those in the treatment group received the pretreatment of polydatin (50μmol/L) for 1 h and were incubated with LPS (5mg/L) for 6h; and those in the inhibitor group received the pretreatment of polydatin (50μmol/L) and silent information regulator 2 related enzyme 3(SIRT3) inhibitor 3-TYP (50μmol/L) for 1h, and were incubated with LPS (5mg/l) for 6h. The cells were then assessed for viability by CCK-8, ATP level by fluorescein-luciferase kits, status of mitochondrial permeability transition pore (mPTP) by Calcein-AM-CoCl2 probe, reactive oxygen species (ROS) level by DCFH-DA fluorescent probe, mitochondrial membrane potential (MMP) by fluorescent probe JC-1, and expression of SIRT3 by Western blotting. SPSS statistics 22.0 was used for data analysis. One-way ANOVA, LSD test or Tamhane′s T2 test was used for comparison among groups. Results Compared with control group, SIRT3 expression in model group decreased to (73.3±4.5)%, JC-1 red/green to (54.0±6.5)%, Calcein fluorescence to (2035±217)U, ATP level to (72.2±4.8)% and cell viability of cells to (73.7±3.7)%, but ROS level increased to (218.0%±21.7)%. Compared with model group, SIRT3 expression in treatment group increased to (86.7±7.6)%, JC-1 red/green [JP+1]to (75.8±7.6)%, Calcein fluorescence to (2571±199)U, ATP level to (86.7±6.3)% and cell viability of cells (83.0±3.6)%, but ROS level decreased to (180.0±18.1)%. Compared with treatment group, SIRT3 expression in inhibitor group decreased to (69.0±7.8)%, JC-1 red/green to (62.8±6.2)%, Calcein fluorescence to (2116±254)U, ATP level to (72.8±5.8)% and cell viability of cells (73.3±4.1)%, but the ROS level increased to (212.0±18.2)%. Conclusion Polydatin alleviates LPS-induced mitochondrial injury in alveolar epithelial cells possibly by the activation of SIRT3.