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目的探讨弓形虫感染孕早期大鼠致胚胎神经系统畸形的分子机制及青蒿素对胚胎的保护作用。方法将SD孕鼠随机分为对照组、模型组和模型治疗组,各组孕鼠于妊娠第3 d(E3)腹腔注射弓形虫RH强毒株,并分别于E12、E14、E16、E18剖腹取胎鼠,进行形态学观察;PCR法检测羊水中弓形虫B1基因表达,免疫荧光染色观察神经细胞粘附分子(NCAM)在胚胎不同发育时期的神经细胞中的表达规律。结果模型组胚胎发育状况差,活胎率低,为11.82%;PCR检测到模型组胚胎羊水B1基因的表达。对照组和模型治疗组E14、E16鼠胚神经细胞中NCAM呈阳性,模型组染色较其他4组弱。结论 NCAM低表达是神经系统畸形发生的重要因素,青蒿素对鼠胚弓形虫感染有保护作用。
Objective To investigate the molecular mechanism of embryonic nervous system deformity caused by Toxoplasma gondii infection in early pregnancy and the protective effect of artemisinin on embryos. Methods Pregnant SD rats were randomly divided into control group, model group and model treatment group. Pregnant mice in each group were injected intraperitoneally with Toxoplasma gondii RH strain on the 3rd day of gestation, and were divided into two groups at the E12, E14, E16 and E18 cesarean section Fetal rats were taken for morphological observation. The expression of B1 gene in amniotic fluid was detected by PCR, and the expression of neural cell adhesion molecule (NCAM) in neural cells at different developmental stages of embryos was observed by immunofluorescence staining. Results The model group had poor embryo development and a low live birth rate of 11.82%. The expression of B1 gene in amniotic fluid of model group was detected by PCR. NCAM positive cells were found in E14 and E16 mouse embryos in model group and control group, and model group was weaker than the other 4 groups. Conclusion Low expression of NCAM is an important factor in the occurrence of nervous system deformity. Artemisinin has a protective effect on Toxoplasma gondii infection.