Objective: To explore the effect of Silent Information Regulator 1 (SIRT1) on cell function of human trabecular meshwork cell (HTMC) under oxidative stress by overexpressing SIRT1 in HTMC. Methods: This is an experiment research. HTMCs were transfected with SIRT1-ovexpressed lentivirus and GFP-negative control lentivirus (Lv-GFP) at the optimal multiplicity of infection (MOI). Real-time quantitative PCR was used to verify whether SIRT1 was overexpressed in HTMC. The following experiments were divided into four groups: normal control group, H₂O₂ group,H₂O₂+Lv-SIRT1-OE group, H₂O₂+Lv-GFP group. Cell migration was detected by transwell assay. Cell viability was detected by CCK8 assay. Student’s t-test was used for two groups. P<0.05 was set as statistical signifificance. Results: The number of migration per well of normal control group, H₂O₂ group, H₂O₂+Lv-SIRT1-OE group, H₂O₂+Lv-GFP group were 436±73,254±25, 510±51, 327±46, respectively. Compared with H₂O₂ group and H₂O₂+Lv-GFP group, transwell assay demonstrated that the number of migrations per well of H₂O₂+Lv-SIRT1-OE group significantly increased (P<0.01). Likewise, CCK8 assay indicated that cell viability of H₂O₂+Lv-SIRT1-OE group was higher than both of H₂O₂ group and H₂O₂+Lv-GFP group (P<0.01). Compared with H₂O₂+Lv-SIRT1-OE group and negative control group (H2O2+Lv-GFP), the expression level of Bax decreased significantly,and the expression level of Bcl-2 increased significantly (P<0.01). ROS assay showed that the ROS level in H₂O₂+Lv-SIRT1-OE group was significantly lower than that in H2O2 group (P<0.05). Conclusion:SIRT1 overexpressed in HTMC can effectively reduce the effect of oxidative stress on migration ability and proliferation activity of HTMC, which lays a foundation for further study on the regulatory mechanism of SIRT1 protecting HTMC under oxidative stress.