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目的通过观察微小RNA-21(mi R-21)在孕鼠胎盘组织的表达,探讨感染性早产的发病机制。方法建立脂多糖诱导的感染性早产模型。孕鼠随机分为对照组、模型组和干预组。对照组腹腔注射生理盐水0.1 m L,模型组腹腔注射脂多糖0.1 m L,干预组腹腔注射脂多糖0.1 m L+20 mg/kg mi R-21模拟物(化学合成的mi R-21)。应用实时荧光定量PCR检测各组胎盘组织中mi R-21的表达,用生物信息学分析方法预测mi R-21的靶点,用免疫组织化学法检测胎盘组织中核因子-κB(NF-κB)蛋白的表达。结果与对照组比较,mi R-21表达在模型组胎盘组织中显著降低,而NF-κB蛋白表达明显升高(P<0.05)。NF-κB是mi R-21的预测靶点,mi R-21模拟物能够下调胎盘绒毛膜组织中NF-κB蛋白表达。结论 mi R-21表达缺失可能参与了感染性早产的发病机制,对以后设计以mi R-21为靶点的特异性药物可能有重要的意义。
Objective To explore the pathogenesis of infective preterm labor by observing the expression of microRNA-21 (mi R-21) in placenta of pregnant rats. Methods Lipopolysaccharide-induced preterm model of infection was established. Pregnant mice were randomly divided into control group, model group and intervention group. The control group received intraperitoneal injection of 0.1 ml saline, while the model group received intraperitoneal injection of lipopolysaccharide 0.1 ml. The intervention group received intraperitoneal injection of 0.1 ml L + 20 mg / kg mi R-21 mimics (chemically synthesized mi R-21). The expression of mi R-21 in placenta of each group was detected by real-time fluorescence quantitative PCR, the target of mi R-21 was predicted by bioinformatics analysis, and the expression of nuclear factor-κB (NF-κB) in placenta was detected by immunohistochemistry Protein expression. Results Compared with the control group, the expression of mi R-21 was significantly decreased in the model group and the expression of NF-κB protein was significantly increased (P <0.05). NF-κB is a predictive target of mi R-21, and mi R-21 mimics down-regulate NF-κB protein expression in placental chorion. Conclusion The lack of mi R-21 expression may be involved in the pathogenesis of infective preterm labor and may be of great significance for the future design of mi R-21-specific drugs.