Abstract
Objective
This study aims to understand the difference of HBxAg and PI3K signal transduction protein expressions in HBV-infected placenta and normal placenta, clarify the difference of the two in the degree of apoptosis and explore the potential role of inhibition of HBxAg/PI3 K/apoptosis in HBV intrauterine infection.
Methods
Placenta tissues of 24 pregnant women with confirmed intrauterine infection and positive HBsAg were selected as the infection group, and those of normal healthy pregnant women were taken as the control group. Immunohistochemical SP staining method was employed to detect the expressions of HBxAg and PI3K in the placenta of each group, and TUNEL was applied for the assay of apoptosis.
Results
HBxAg was detected in the placenta of HBV-infected group, and staining optical density value of high replication group (HBV DNA >1 × 103 copies/mL) was higher than that of low replication group (HBV DNA <1 × 103 copies/mL), and there was statistical significance (p < 0.05); PI3K expression levels in the placenta of HBV-infected groups were higher than that of the control group and there was statistical significance (p < 0.01), and staining optical density value of high replication group was higher than that of low replication group and it was statistically significant (p < 0.01); apoptosis index of HBV-infected high replication group was lower than that of low replication group and control group and there was statistical significance (p < 0.01).
Conclusion
HBV infected placenta tissues and then produced functional proteins HBxAg in trophoblast cells, and HBxAg/PI3 K/anti-apoptosis is the potential mechanism for pregnant women with HBV DNA high replication to have intrauterine infection while there exists different mechanism for pregnant women with negative HBV DNA.
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Bai, G., Wang, Y., Zhang, L. et al. The study on the role of Hepatitis B virus X protein and apoptosis in HBV intrauterine infection. Arch Gynecol Obstet 285, 943–949 (2012). https://doi.org/10.1007/s00404-011-2096-2
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DOI: https://doi.org/10.1007/s00404-011-2096-2