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目的研究孕期染汞胎鼠脑组织的损伤情况,探讨S100B在胎鼠脑损伤中的表达及意义。方法建立孕鼠动物模型,将孕鼠随机分为对照组及染汞组(0.8、1.4、2.0mg·kg~(-1)·d~(-1));染汞组于妊娠6-9 d连续灌胃给药,对照组为蒸馏水同期灌胃。妊娠第19天用戊巴比妥钠(40mg/kg)麻醉孕鼠,剖腹取胎。应用电感耦合等离子体质谱法(ICP-MS)测定各组胎鼠脑组织汞含量;酶联免疫吸附实验(ELISA)检测各组胎鼠脑组织中S100B水平;脱氧核糖核苷酸末端转移酶介导的缺口末端标记法(TUNEL)法检测各组胎鼠脑细胞凋亡情况;蛋白印迹法(Western blot)检测各组胎鼠脑组织bcl-2蛋白表达情况。结果 0.8 mg·kg~(-1)·d~(-1)、1.4 mg·kg~(-1)·d~(-1)及2.0mg·kg~(-1)·d~(-1)浓度的氯化甲基汞组,胎鼠脑组织中S100B蛋白的水平分别为(0.43±0.03)μg·L~(-1)、(0.62±0.03)μg·L~(-1)、(0.64±0.03)μg·L~(-1),呈增加趋势。胎鼠脑组织的汞含量较对照组明显升高(P<0.05),S100B蛋白的表达量与对照组比较的差异有统计学意义P<0.05);胎鼠的脑细胞凋亡率较对照组也明显升高(P<0.05),实验组(染汞组)的bcl-2蛋白表达量较对照组则有明显下降(P<0.05)。结论孕期染汞可导致胎鼠脑细胞凋亡增加,脑组织中S100B蛋白水平升高,提示S100B可成为孕期汞暴露胎鼠脑损伤的预测指标。
Objective To study the injury of brain tissue during pregnancy with mercury-enriched fetal rat and to explore the expression and significance of S100B in fetal brain injury. Methods The animal model of pregnant rats was established. Pregnant mice were randomly divided into control group and mercury-stained group (0.8, 1.4, 2.0 mg · kg -1 · d -1) d continuous oral administration, the control group of distilled water over the same gavage. Pregnant rats were anesthetized with sodium pentobarbital (40 mg / kg) on day 19 of gestation, and cesarean section was taken. The content of mercury in fetal rat brain tissue was measured by inductively coupled plasma mass spectrometry (ICP-MS). The level of S100B in fetal rat brain tissue was detected by enzyme linked immunosorbent assay (ELISA) TUNEL method was used to detect the apoptosis of brain cells in each group. Western blot was used to detect the expression of bcl-2 protein in fetal rat brain tissue. Results After treatment with 0.8 mg · kg -1 · d -1, 1.4 mg · kg -1 · d -1 and 2.0 mg · kg -1 · d -1 (0.43 ± 0.03) μg · L -1 and (0.62 ± 0.03) μg · L -1, respectively, and the level of S100B protein in fetal rat brain tissue was 0.64 ± 0.03) μg · L -1, showing an increasing trend. The content of mercury in fetal brain tissue was significantly higher than that in the control group (P <0.05), the expression level of S100B protein in the control group was significantly higher than that in the control group (P <0.05) (P <0.05). The expression of bcl-2 protein in experimental group was significantly lower than that in control group (P <0.05). Conclusions Mercury exposure during pregnancy may lead to increased apoptosis of brain cells in fetal rat brain and increase of S100B protein in brain tissue, which suggests that S100B may be a predictor of brain injury during fetal exposure to mercury.