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目的:初步探讨糖原合成激酶3β(GSK3β)与乙肝病毒胎盘组织感染关系,为进一步研究乙肝病毒在宫内感染中的作用机制奠定基础。方法:选择2011年-2012年在哈尔滨医科大学附属第二医院妇产科剖宫产结束妊娠的乙肝表面抗原阳性(HBsAg+)孕妇60例(实验组),正常妊娠孕妇的胎盘组织20例(对照组)。于分娩前留取孕妇肘静脉血,分娩时留取脐血及胎盘组织。采用ELISA法检测实验组静脉血及脐带血的乙肝五项与HBV-DNA定量;采用免疫组化方法,检测各实验组中HBsAg的表达及分布;检测实验组与对照组GSK3β的分布及表达情况;采用TUNEL法检测实验组及对照组细胞凋亡情况。结果:60例HBsAg(+)产妇中,37例脐带血HBsAg阳性,12例脐带血HBV-DNA阳性;实验组胎盘组织中均检测出HBsAg、GSK3β蛋白表达,且随着血清HBV-DNA滴度增高,HBsAg与GSK3β的表达均呈增高趋势(P<0.05);实验组和对照组的胎盘组织中均可检测出凋亡细胞,实验组的凋亡程度低于对照组,随HBV-DNA滴度增高,凋亡呈下降趋势(P<0.05)。结论:在乙肝病毒的垂直传播过程,HBsAg可能通过GSK3β抑制胎盘细胞凋亡,影响正常胎盘组织的屏障功能,可能是造成宫内感染的相关机制。
Objective: To investigate the relationship between glycogen synthesis kinase 3β (GSK3β) and hepatitis B virus (HBV) placental tissue infection, and to lay a foundation for further study on the mechanism of hepatitis B virus infection in intrauterine infection. Methods: Sixty pregnant women (experimental group) with HBsAg positive (HBsAg +) were enrolled in the Department of Obstetrics and Gynecology of the Second Affiliated Hospital of Harbin Medical University from 2011 to 2012. Twenty placenta tissues of normal pregnant women group). Pregnant women were given elbow venous blood before delivery and cord blood and placental tissue were taken during childbirth. Immunohistochemistry was used to detect the expression and distribution of HBsAg in each experimental group. The distribution and expression of GSK3β in the experimental group and the control group were detected TUNEL method was used to detect the apoptosis in experimental and control groups. Results: In 60 cases of HBsAg (+) mothers, 37 cases of umbilical cord blood HBsAg positive and 12 cases of cord blood HBV-DNA positive; HBsAg and GSK3βprotein were detected in placenta of experimental group, and with the serum HBV-DNA titer (P <0.05). Apoptotic cells could be detected in both placenta and placenta of experimental group and control group. The degree of apoptosis in the experimental group was lower than that in the control group, with the increase of HBV-DNA Degree increased, apoptosis showed a downward trend (P <0.05). Conclusion: In the process of vertical transmission of hepatitis B virus, HBsAg may inhibit placental cell apoptosis through GSK3β and affect the barrier function of normal placenta tissue, which may be the related mechanism of intrauterine infection.