Background and Objective; Peroxiredoxins (Prxs) are important proteins in redox system and its molecular effect in cardiovascular cell lines are still ambiguous. Methods; We investigated expression pattern of Prxs in neonatal rat cardiomyocytes (rCMCs), rat vascular smooth muscle cells (VSMCs) and human umbilical vein endothelial cells (HUVECs) with H₂O₂. Under the 0.1 mM of H₂O₂, 3 cell lines were incubated for 30, 120 minute, we evaluated the expression pattern of six Prx isoforms and apoptosis by Western blot and flowcytometry (FACS). Prx1 protective effect in rCMC from apoptosis under H₂O₂ was investigated with gene delivery of Prx1. rCMCs were infected by Lenti(lenti-viral)-Prx1 and GFP. Oxidative stress was added to rCMCs with 0.25 mM H₂O₂. Degrees of apoptosis, Prx1 and survival signal expression were evaluated with FACS, Western blot and Immunohistochemistry (IHC). Results; H₂O₂ (0.1 mM)-induced increased apoptotic cell death compared to control on 2 hrs. After H₂O₂ adding, Prx2, 3 expressions were decreased but Prx1, 6 expressions were up-regulated in rCMC. In VSMCs, all Prxs was increased significantly than control. In HUVECs, Prx1, 5 was up-regulated whereas Prx2, 3, 4 and 6 were not changed. Expression of Prx1 was increased in rCMCs/Lenti-Prx1 with H₂O₂ than rCMCs/Lenti-GFP with H₂O₂. Lenti-Prx1 gene delivery effectively reduced apoptosis in rCMC under oxidative stress was created by H₂O₂. Expression of caspase 3 was increased rCMCs/Lenti-GFP with H₂O₂. Conclusion; The molecular and cellular changes in rCMC, VSMC and HUVEC related with H₂O₂-induced oxidative stress and Prx isoform expression was very dynamic. And our results proved that the Prx1 signaling network plays an important role in regulating cardiovascular cell viability.