Department of Gynecology and Obstetrics, The First Affiliated Hospital of Medical College of Xi'an Jiaotong University, Jiankang Road No.1, Xi'an 710061, Shaanxi, China.
Arch Gynecol Obstet. 2012 Apr;285(4):943-9. doi: 10.1007/s00404-011-2096-2. Epub 2011 Oct 11.
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.
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.
HBxAg was detected in the placenta of HBV-infected group, and staining optical density value of high replication group (HBV DNA >1 × 10(3) copies/mL) was higher than that of low replication group (HBV DNA <1 × 10(3) 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).
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.
本研究旨在了解 HBV 感染胎盘与正常胎盘组织中 HBxAg 和 PI3K 信号转导蛋白表达的差异，阐明两者在细胞凋亡程度上的差异，并探讨抑制 HBxAg/PI3K/凋亡在 HBV 宫内感染中的潜在作用。
选择 24 例 HBsAg 阳性、确诊宫内感染的孕妇胎盘组织作为感染组，正常健康孕妇胎盘组织作为对照组。采用免疫组化 SP 染色法检测两组胎盘组织中 HBxAg 和 PI3K 的表达，TUNEL 法检测凋亡。
HBV 感染组胎盘组织中检测到 HBxAg，高复制组（HBV DNA＞1×10³拷贝/ml）HBxAg 染色光密度值高于低复制组（HBV DNA＜1×10³拷贝/ml），差异有统计学意义（p＜0.05）；HBV 感染组胎盘组织中 PI3K 表达水平高于对照组，差异有统计学意义（p＜0.01），且高复制组染色光密度值高于低复制组，差异有统计学意义（p＜0.01）；HBV 感染高复制组的凋亡指数低于低复制组和对照组，差异有统计学意义（p＜0.01）。
HBV 感染胎盘组织后在滋养细胞中产生功能性蛋白 HBxAg，HBxAg/PI3K/抗凋亡可能是 HBV DNA 高复制孕妇发生宫内感染的潜在机制，而 HBV DNA 阴性孕妇可能存在不同的机制。
