Objective To investigate the expression of MicroRNA⁃27a（miR⁃27a）in the placenta of gesta⁃ tional diabetes mellitus（GDM）rats and its effects on oxidative stress and inflammation in GDM rats，as well as to analyze the underlying mechanism. Methods SD normal pregnant rats were injected intraperitoneally with strepto⁃ zotocin（STZ）to induce the establishment of GDM models. After successful modeling，they were divided into four groups：model group，agomir ⁃NC group，miR ⁃27a agomir group，and miR ⁃27a agomir + lipopolysaccharide（LPS） group，eachwith 12 rats；the control group consisted of12 normal pregnant rats. The levels of fasting blood glucose （FBG）and fasting insulin（FINS）in rats were detected，and the insulin resistance index（HOMA⁃IR）was calculated； the pregnancy outcome and placenta quality were analyzed；the levels of interleukin 1β（IL⁃1β）and tumor necrosis factor α（TNF⁃α），the activities of superoxide dismutase（SOD）and catalase（CAT），and the content of malondialde⁃ hyde（MDA）in placenta tissuewere determined；Hematoxylin⁃Eosin（HE）staining and TUNEL method were used to detect pancreatic and placental tissue damage and cell apoptosis；and real ⁃time quantitative PCR（RT ⁃ qPCR）and Western blot were used to detect the levels of miR⁃27a，Toll⁃like receptor 4（TLR4），myeloid differentiation factor 88 （MyD88），nuclear factor⁃κB p65（NF⁃κB p65）mRNAs and proteins in placental tissues. Results Overexpression of miR⁃27a significantly reduced FBG，FINS and HOMA⁃IR in GDM rats，accompanied by a reduction in pro⁃inflam⁃ matory cytokine levels and oxidative stress，improved placental and pancreatic tissue damage and apoptosis，and the pregnancy outcome，and inhibited the activation of the TLR4/MyD88/NF ⁃κB signaling pathway in the placenta （P < 0.05）. Conclusion The overexpression of miR ⁃27a can reduce the placental inflammation，oxidative stress， and IRin GDM rats. Its mechanism could be related to the inhibition of the TLR4/MyD88/NF⁃κB signaling pathway