Objective To investigate the effects of oxidative stress on human uterine ligament fibroblast proliferation, apoptosis, collagen synthesis and expression of inflammatory factors. Methods Third generation rat uterine ligament fibroblasts were divided into low oxidative stress, high oxidative stress and control groups. Hydrogen peroxide at 0. 2 mmol / L and 0. 8 mmol / L was applied to uterine ligament fibroblasts for 4 h to establish low and high level oxidative stress models, respectively. The methyl thiazolyl tetrazolium(MTT) assay was used to detect cell proliferation, the Annexin V-fluorescein isothiocyanate / propidium iodide(V-FITC/ PI) method was applied to detect apoptosis, and Western blot was used to detect the protein levels of type I collagen, type III collagen, inflammatory factors and signal pathway-related proteins. Results Compared with the control and low oxidative stress groups, the proliferation ability of cells in the high oxidative stress group was decreased (P<0. 05), the apoptosis rate was increased (P<0. 05), the synthesis of type I and type III collagen was decreased (P<0. 05), and the protein expression levels of interleukin ( IL) -1β, tumour necrosis factor alpha(TNF-α) and IL-6 were increased (P< 0.05). Compared with the control and low oxidative stress groups, phosphorylated-extracellular signal-regulated kinase 1 / 2(ERK1 / 2) and phosphorylated- protein kinase B(Akt) expression in the high oxidative stress group was decreased (P< 0. 05), whereas the expression of total protein ERK1 / 2 and Akt remained almost unchanged. There were no significant difference between the low oxidative stress and control groups. Conclusions A high hydrogen peroxide concentration in an oxidative stress microenvironment can inhibit ERK1 / 2 expression in the MAPK pathway and Akt expression in the phosphoinositide 3-kinase(PI3K) / Akt pathway, resultsing in decreased uterine ligament fibroblast proliferation and collagen synthesis and increased expression of apoptotic cells and inflammatory factors, which may participate in the occurrence and development of pelvic organ prolapse.