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孕期酒精暴露诱导仔鼠胰岛素抵抗与海马应激损伤 被引量:2
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作者 周淑芳 高林 +2 位作者 贺维亚 崔占军 邓锦波 《解剖学报》 CAS CSCD 北大核心 2014年第1期7-14,共8页
目的探讨在孕期酒精暴露模型中胰岛素抵抗与海马应激损伤的相关性及其机制。方法利用C57BL/6J小鼠建立孕期酒精暴露模型,分为对照组、中剂量组和高剂量组;对各组出生第7天(P7)、P14、P30仔鼠进行空腹血糖和空腹血胰岛素测定并计算胰岛... 目的探讨在孕期酒精暴露模型中胰岛素抵抗与海马应激损伤的相关性及其机制。方法利用C57BL/6J小鼠建立孕期酒精暴露模型,分为对照组、中剂量组和高剂量组;对各组出生第7天(P7)、P14、P30仔鼠进行空腹血糖和空腹血胰岛素测定并计算胰岛素抵抗指数;利用免疫荧光染色法观察各组年龄点仔鼠海马CA1区细胞应激损伤指标c-Fos、核因子-κB(NF-κB)及炎症因子环氧合酶-2(COX2)的阳性细胞数;免疫印迹法检测P7、P14仔鼠海马组织c-Fos、NF-κB激活蛋白的相对表达量以印证免疫荧光染色结果。结果酒精暴露后仔鼠胰岛素抵抗指数升高,且具有酒精剂量依赖性(P<0.05,n=90);酒精暴露后各年龄点仔鼠海马组织CA1区应激损伤指标c-Fos、NF-κB和炎症因子COX2阳性细胞数增多,存在酒精剂量依赖性(P<0.05,n=90)和长时程效应;孕期酒精暴露后海马组织c-Fos、NF-κB激活蛋白表达量增多(P<0.05,n=30),同时存在酒精剂量依赖性和长时程效应,与免疫荧光结果一致。结论孕期酒精暴露可诱导仔鼠产生胰岛素抵抗,其原因可能是氧化应激的结果;胰岛素抵抗可能参与胎儿酒精综合症大脑损伤及其发病机制,c-Fos、NF-κB通路可能是胰岛素抵抗损伤大脑的分子机制之一。 展开更多
关键词 孕期酒精暴露 胰岛素抵抗 氧化应激 海马 应激损伤 免疫荧光法 免疫印迹法 小鼠
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The Detection of 1-Palmitoyl-2-oleoyl-<i>sn</i>-glycero-3-phosphoethanol and Ethyl Glucuronide in Human Umbilical Cord
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作者 Joseph Jones Mary Jones +1 位作者 Charles Plate Douglas Lewis 《American Journal of Analytical Chemistry》 2012年第12期800-810,共11页
In utero exposure to ethanol continues to be a significant public health issue and neonatal healthcare professionals are in need of objective means to identify exposed newborns. The aim of this study was to fully vali... In utero exposure to ethanol continues to be a significant public health issue and neonatal healthcare professionals are in need of objective means to identify exposed newborns. The aim of this study was to fully validate two methods for the detection of two direct alcohol biomarkers, 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphoethanol (POPE) and ethyl glucuronide (EtG), in umbilical cord and apply the assays to a group of authentic specimens. The limits of detections were 2 and 1 ng/g for POPE and ETG and the limits of quantitation were 4 and 3 ng/g, respectively. Inter and intra-day precision and accuracy measurements were within 15%. The assays were applied to 308 authentic specimens where we detected POPE in five (1.6%) specimens and EtG in twelve (3.9%) specimens. The mean concentrations were 11.4 ng/g ± 9.4 ng/g and 127.2 ± 227.7 ng/g for POPE and EtG, respectively. This study suggested that umbilical cord was a suitable specimen type for the identification of newborns exposed to ethanol in the womb and the prevalence of POPE and EtG detected in umbilical cord were consistent with the prevalence of self-reported binge drinking reported by the National Birth Defect Prevention Study (NBDPS) and Behavioral Risk Factor Surveillance System (BRFSS). Further studies are required to fully describe the association between the observed concentrations of POPE and EtG in umbilical cord to the level of maternal consumption of ethanol. 展开更多
关键词 PHOSPHATIDYLethanol Ethyl GLUCURONIDE Umbilical Cord ethanol FETUS LC-MS/MS prenatal exposure Fetal Alcohol Spectrum Disorders FASD
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孕期乙醇暴露所致高脂饮食子代大鼠糖代谢功能改变 被引量:1
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作者 李霞 肖笛 +4 位作者 寇皓 张郦 纪振宇 郭喻 汪晖 《中国临床药理学与治疗学》 CAS CSCD 2017年第1期20-26,共7页
目的:观察孕期乙醇暴露(prenatal ethanol exposure,PEE)对高脂饮食诱导下的成年子代糖代谢功能的影响。方法:Wistar孕鼠自受孕11 d灌胃给予乙醇(4 g·kg^(-1)·d^(-1))或等容量生理盐水至分娩。仔鼠断奶后均给予高脂饮食,于出... 目的:观察孕期乙醇暴露(prenatal ethanol exposure,PEE)对高脂饮食诱导下的成年子代糖代谢功能的影响。方法:Wistar孕鼠自受孕11 d灌胃给予乙醇(4 g·kg^(-1)·d^(-1))或等容量生理盐水至分娩。仔鼠断奶后均给予高脂饮食,于出生后第20周(postnatal week 20,PW20)行糖耐量实验。PW24处死动物并检测胰腺病理形态,取肝脏检测胰岛素信号通路关键基因的mRNA表达。结果:与对照组相比,PEE子代PW1体质量均降低(P<0.01),出生后体质量增长率显著升高(P<0.01),且胰岛病理损伤更为明显;PEE子代基础血胰岛素较对照组低,给予糖负荷后,雄、雌子代血胰岛素分泌明显增加,但绝对胰岛素水平仍低于对照组。PEE组雌性子代胰岛素敏感指数增加(P<0.05),但糖耐量异常;PEE子代肝脏胰岛素信号通路关键基因mRNA水平显著升高(P<0.05)。结论:PEE子代在高脂饮食诱导下出现追赶性生长,胰腺糖代谢功能下降但仍有代偿作用,肝脏胰岛素敏感性增加,以雌性更为明显。 展开更多
关键词 糖代谢功能 高脂饮食 孕期乙醇暴露
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