关键词: 地塞米松, 葡萄糖, 糖皮质激素受体, 葡萄糖转运蛋白, 活性氧

Abstract:

AIM: To explore the effect and mechanism of dexamethasone (DEX) on the function of placental transport of glucose. METHODS: One hundred and sixty premature pregnant women who received treatment and delivery in Hangzhou First People's Hospital were randomly divided into control group and DEX group (n=80). Ten placenta tissue samples were randomly selected from two groups, respectively. Immunohistochemistry was used to detect human placental lactogen. JEG-3 cell line used to research mechanism was divided into 4 groups according to different transfer vectors, i.e group pcDNA3.1, group pcDNA3.1-GRα, group Control siRNA and group GRα siRNA. The CCK-8 method was used to detect placental cell proliferation. TUNEL method was used to detect degree of apoptosis. Mitochondrial membrane potential (MMP) and glucose uptake were detected. Fluorescent probe was used to detect content of reactive oxygen species. Quantitative real-time polymerase chain reaction was used to detect the relative the expression level of GRα and GLUT.RESULTS:The strong expression of HPL in control group was more than that in DEX group. Compared with pcDNA3.1 group, cell proliferation, MMP level and glucose uptake increased significantly in pcDNA3.1-GRα group (P<0.05, P<0.01); yet cell apoptosis and reactive oxygen species (ROS) level decreased significantly (P<0.01) and the relative expression level of GRα, GLUT1 and GLUT3 increased significantly (P<0.01). Compared with control siRNA group, cell proliferation, MMP level and glucose uptake of GRα siRNA group decreased significantly (P<0.05, P<0.01); yet cell apoptosis and ROS level increased significantly (P<0.01) and the relative expression level of GRα, GLUT1 and GLUT3 decreased significantly (P<0.05). CONCLUSION: DEX can induce glucose transport function of placenta, which is likely related with ROS/AMPK pathway.

Key words: dexamethasone, glucose, glucocorticoid receptor, glucose transporter, reactive oxygen species