Aim The aim of this study is to investigate the effects of SGI-1776 on the proliferation of HUSAEC cell induced by H₂O₂ oxidative stress and its possible molecular mechanism. Methods HUSAEC cells were cultured in vitro. The cells which would be induced by H₂O₂ were incubated in advance for 30 minutes with catalase （CAT） and various concentration of SGI-1776（2.5, 5 and 10 μmoL/L）. Cells viability was measured by MTT assay, and its cell cycle phase and apoptotic rate were determined by FCM with PI staining, meanwhile western blot assay and SiRNA /cDNA assay were used to examine the possible mechanism of SGI-1776 on promoting proliferation action of HUSAEC Cell induced by H₂O₂ oxidative stress. Results SGI-1776 could increase the viability of HUSAEC cells induced by H₂O₂ in a dose and time-dependent manner compared with cells solo exposed to H₂O₂ （P<005）. The cell cycle phase of G₂/M was reduced and the apoptotic rate of HUSAEC cells treated with various concentration SGI-1776 significantly decreased in a dose and time-dependent manner compared with H₂O₂ group（P<0.05）, meanwhile the expression of cortactin protein were up-regulated in a dose and time-dependent manner（P<0.05）. siRAN could interfere with cortactin protein expression, and SGI-1776 could counteract the effect of down-regulation of cortactin of siRAN. Transferring cDNA could up-regulate cortactin protein expression, and it posed synergetic action with SGI-1776. Conclusion SGI-1776 could enhance the proliferation viability of H₂O₂-induced HUSAEC cells which may be related to up-regulating the cortactin protein expression to help H₂O₂-induced HUSAEC cells out G₂/M block, and reduce apoptotic rate.