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机构地区:[1]金华市人民医院生殖中心,金华321000 [2]武义县中医院,金华321200 [3]浙江大学医学院附属妇产科医院中心实验室,杭州310012
出 处:《生殖医学杂志》2016年第1期56-60,共5页Journal of Reproductive Medicine
基 金:金华市科技计划项目(No.2014A33503)
摘 要:目的建立输卵管炎模型,检测Toll样受体-2(TLR2)和肿瘤坏死因子-α(TNF-α)的表达,探讨其与输卵管炎的关系。方法 48只6~8周龄BALB/c雌性小鼠,随机平均分为空白组(不处理)和模型组(子宫底注入l×109/ml金黄色葡萄球菌悬液50μl)。分别在接种3d、7d、14d、28d处死模型组和对应时间的空白组小鼠,收集血液和输卵管。采用实时荧光定量PCR检测输卵管组织TLR2mRNA以及ELISA检测血TNF-α在模型组和相应空白组中的表达,并观察各组输卵管病理改变。结果空白组各时间点输卵管组织TLR2mRNA表达及血TNF-α浓度均无显著差异(P〉0.05);模型组3d、7d、14d时TLR2mRNA表达逐渐降低,TNF-α浓度逐渐升高,但均无统计学差异(P〉0.05),而28d时TLR2mRNA相对表达含量(0.822)显著低于3d时(1.296)(P〈0.05);模型组各时间点血清TNF-α水平均显著高于相应空白组(P〈0.05)。结论TLR2可能通过一系列信号转导,诱导产生大量TNF-α,引起输卵管炎。Objective: To establish a salpingitis model for exploring the association between toll like receptor-2 (TLR2) & tumor necrosis factor-α (TNF-α) and salpingitis. Methods: Forty-eight BALB/c female mice of 6-8 weeks were randomly divided to control group and model group. The mice in control group had no treatment,and the fundus of uterus of mice in model group was injected 50 μ 1× 109/ml suspension of staphylococcus aureus. The blood and fallopian tubes were collected after 3,7,14,28 days of treatment. The expressions of TLR2 mRNA in fallopian tubes and serum TNF-α levels were detected by using real-time fluorescence quantitative PCR and ELISA,respectively, and the pathological changes of fallopian tubes were observed in the model group and control group. Results: The expressions of TLR2 mRNA and serum TNF-α levels were not significantly different along with the time in the control group (P〉0.05). The expressions of TLR2 mRNA were gradually decreased,while the concentrations of TNF-α were gradually increased after 3,7,14 days of treatment, but there were no significant differences (P〉0.05). The TLR2 mRNA expression after 28 days of treatment was significantly lower than that after 3 days of treatment (P〈0.05). The serum TNF-α levels in model group were all significantly higher than those in control group at corresponding time points (P〈0. 05). Conclusions.. TLR2 might induce more TNF-α production through a series of signal pathways to cause salpingitis.
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