Objective To study the role of cysteine aspartic acid-specific protease-3 (caspase-3),matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of matrix metallo proteinase-2 (TIMP-2) in human amniochorionic membranes during premature rupture of humanfetal membranes (PROM).Methods Amniochorionic membranes were collected from the following groups ofwomen: women with spontaneous PROM (n=8), women with normal labor in termafter vaginal delivery(n=8) and women undergoing elective repeat cesarean section(C-section) before the onset of labor and who had no complications of pregnancy(n=8). Caspase-3 peptides were studies with use of immunohistochemistry. Messengerribonucleic acid (mRNA) expression for MMP-2 and its specific inhibitors TIMP-2was studied with use of reverse transcriptase-polymerase chain reaction (RT-PCR).Results 1) The expressions of Caspase-3 peptides were 62.86 ± 3.83% in PROMgroup, 42.33 ± 2.99% in vaginal delivery group, and 20.97 ± 2.94% in C- sectiongroup. There were statistically significant changes among the three groups (P<0.05).Immunohistochemistry demonstrated the presence of Caspase-3 in the amniotic epithelialcells and chorionic cytotrophoblast cells. 2) The expressions of MMP-2 were 84.92 ±3.68% in PROM group, 32.65 ± 2.34% in vaginal delivery group, and 30.65 ±2.77% in C-section group. There were statistically significant changes between PROMand C-section group (P<0.05). 3) The expressions of TIMP-2 were 42.01 ± 12.17% inPROM group, 73.01 ± 14.82% in vaginal delivery group, and 88.47 ± 6.51% inC- section group. There were statistically significant changes among the three groups(P<0.05).Conclusion Caspase-3 gene expressed more in PROM than in comparative group,which caused human fetal membranes cell apoptosis increased. The expression MMP-2increased and TIMP-2 dropped in PROM, which can increase the ECM decomposing.Cell apoptosis increased and extra cellular matrix degradation dropped, which maycause weakening of the membrane’s elasticity and tenacity, then lead to PROM. Objective To study the role of cysteine ​​aspartic acid-specific protease-3, matrix metalloproteinase-2 (MMP-2) and tissue inhibitor of matrix metallo proteinase-2 (TIMP-2) in human amniochorionic membranes during premature rupture of humanfetal membranes (PROM). Methods Amniochorionic membranes were collected from the following groups of women: women with spontaneous PROM (n = 8), women with normal labor in termafter vaginal delivery (n = 8) and women undergoing elective repeat cesarean section -section) before the onset of labor and who had no complications of pregnancy (n = 8). Caspase-3 peptides were studies with use of immunohistochemistry. Messenger ribonucleic acid (mRNA) expression for MMP-2 and its specific inhibitors TIMP- Results 1) The expressions of Caspase-3 peptides were 62.86 ± 3.83% in PROMgroup, 42.33 ± 2.99% in vaginal delivery group, and 20.97 ± 2.94% in C- sectiongroup. There were st Of the significant changes among the three groups (P <0.05). Immunohistochemistry demonstrated the presence of Caspase-3 in the amniotic epithelial cells and chorionic cytotrophoblast cells. 2) The expressions of MMP-2 were 84.92 ± 3.68% in PROM group, 32.65 ± 2.34 There was statistically significant changes between the PROM and C-section groups (P <0.05) .3) The expressions of TIMP-2 were 42.01 ± 12.17% inPROM group, There were statistically significant changes among the three groups (P <0.05) .Conclusion Caspase-3 gene expressed more in PROM than in comparative group, which caused human fetal membranes cell apoptosis increased. The expression MMP-2 increased and TIMP-2 dropped in PROM, which can increase the ECM decomposing. Cell apoptosis increased and extra cellular matrix degradation dropped, which may cause weakening of the membrane’s elasti city ​​and tenacity, then lead to PROM.