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目的观察弓形虫感染妊娠中期的BALB/c小鼠后,对胎盘组织中细胞凋亡相关蛋白Bax、Bcl-2、Fas、FasL及TNF-α表达的影响,探讨弓形虫感染导致细胞凋亡增加的可能机制。方法在妊娠第8d,实验组经腹腔无菌接种纯化的弓形虫速殖子100个,溶于0.2mL PBS;对照组注射等量无菌PBS(0.01mol/L,pH=7.4)。于妊娠第12、14、16、18d,随机处死实验组和对照组孕鼠各5只,采用免疫组织化学法(i mmunohistochemistry)检测胎盘组织中细胞凋亡相关蛋白Bax、Bcl-2、Fas、FasL及TNF-α的表达水平。结果免疫组化显示,细胞凋亡相关蛋白在胎盘绒毛和蜕膜组织中均有表达,以胎盘合体滋养细胞表达较多。Bax、Fas、FasL及TNF-α的表达量实验组和对照组均随着妊娠期的延长而增加,相同妊娠天数实验组的表达量均比对照组多。Bcl-2的表达量均随着妊娠期的延长而减少,相同妊娠天数实验组的表达量均比对照组少。结论弓形虫感染妊娠中期的小鼠,可引起胎盘组织中细胞凋亡相关蛋白表达量的改变,进而启动内、外源性的细胞凋亡途径,导致胎盘细胞凋亡增加。
Objective To investigate the effect of Toxoplasma gondii infection on the expression of Bax, Bcl-2, Fas, FasL and TNF-α in placenta of BALB / c mice infected with Toxoplasma gondii in the second trimester of pregnancy. Possible mechanism. Methods On the 8th day of gestation, 100 rabbits of Toxoplasma gondii were inoculated intraperitoneally in the experimental group and dissolved in 0.2mL PBS. The control group was injected with equal volume of sterile PBS (0.01mol / L, pH = 7.4). On the 12th, 14th, 16th and 18th day of gestation, 5 pregnant rats were randomly sacrificed and the apoptosis-related proteins Bax, Bcl-2 and Fas were detected by immunohistochemistry (i mmunohistochemistry) FasL and TNF-α expression levels. Results Immunohistochemistry showed that apoptosis-related proteins were expressed in placental villi and decidua, and were expressed in placental syncytiotrophoblasts. The expression of Bax, Fas, FasL and TNF-α in the experimental group and the control group increased with the extension of gestation. The expression of Bax, Fas, FasL and TNF-α in the experimental group was higher than that in the control group in the same gestational days. The expression of Bcl-2 decreased with the extension of gestation, and the expression of Bcl-2 in experimental group was less than that in control group in the same gestational days. Conclusion Toxoplasma gondii infects mice in the second trimester of pregnancy and induces changes in the expression of apoptosis-related proteins in placental tissue, which in turn triggers both endogenous and exogenous apoptotic pathways leading to increased placental apoptosis.