小胶质细胞在大鼠子痫前期模型后代胎脑中的激活

目的 观察子痫前期大鼠后代胎脑前额叶皮质、海马及小脑中小胶质细胞变化情况。方法 通过缩窄腹主动脉及双侧子宫动脉,制造子宫胎盘缺血模型(RUPP),检测20.5 d孕鼠动脉血压,尿总蛋白及肾脏病理改变。免疫荧光染色和Western blot检测胎脑前额叶皮质、海马及小脑内小胶质细胞标记分子Iba1的表达。结果 动脉血压检测结果显示,RUPP组动脉血压显著高于对照组。HE染色结果显示,与对照组相比,RUPP组肾小球细胞体积增大,肾小球内细胞数目增多。Western blot结果显示,与对照组相比,RUPP组胎脑前额叶皮质Iba1蛋白表达增多,但是在海马及小脑无明显改变。免疫荧光染色结果显示,与对照组相比,RUPP组胎脑前额叶皮质Iba1数量增多,但是在海马及小脑无明显改变。结论 子痫前期导致胎脑前额叶皮质小胶质细胞增生可能是子代神经发育异常的部分原因。     

硫酸镁对子痫前期大鼠胎盘组织氧化应激损伤和低氧诱导因子1α表达水平的影响

目的探讨硫酸镁对子痫前期大鼠胎盘组织氧化应激损伤及低氧诱导因子1α(HIF⁃1α)表达水平的影响。方法将30只SD大鼠随机分为空白对照组、子痫前期(PE)组、硫酸镁组各10只,除空白对照组外,均采用内毒素构建PE大鼠模型,硫酸镁组给予硫酸镁80 mg/kg腹腔注射干预,空白对照组、PE组注射同等剂量生理盐水,孕21 d行剖宫产,分离胎盘组织,采用荧光定量聚合酶链反应法(RT⁃PCR)法测定胎盘组织HIF⁃1α水平,并采用紫外比色法测定胎盘组谷胱甘肽过氧化物酶(GPX)、丙二醛(MDA)、超氧化物歧化酶(SOD)水平,采用组织匀浆法测定胎盘组织活性氧(ROS)水平。结果(1)妊娠10 d,各组血压、24 h尿蛋白定量比较差异无统计学意义(均P>0.05),妊娠15 d、妊娠21 d,空白对照组血压、24 h尿蛋白定量无明显变化,PE组、硫酸镁组上述指标均上升(均P<0.05),与同组妊娠10 d比较差异有统计学意义(均P<0.05),且高于空白对照组同时间段血压、24 h尿蛋白定量(均P<0.05),硫酸镁组妊娠21 d血压及24 h尿蛋白定量均低于PE组(均P<0.05);(2)PE组大鼠胎盘质量、仔鼠体质量及身长均低于空白对照组(均P<0.05),硫酸镁组大鼠胎盘质量、仔鼠体质量及身长高于PE组(均P<0.05);(3)PE组、硫酸镁组胎盘组织GPX、SOD均低于空白对照组(均P<0.05),MDA、ROS、HIF⁃1αmRNA高于空白对照组(均P<0.05),硫酸镁组胎盘组织GPX、SOD高于PE组,MDA、ROS、HIF⁃1αmRNA低于PE组(均P<0.05)。结论PE大鼠伴明显氧化应激损伤,且胎盘组织HIF⁃1αmRNA水平较高,而给予硫酸镁干预可减轻其氧化应激损伤,下调HIF⁃1αmRNA表达。     

C1q和肿瘤坏死因子相关蛋白4(CTRP4)降低子痫前期大鼠滋养层细胞的caspase-1和IL-1β水平

目的探讨C1q和肿瘤坏死因子相关蛋白4(CTRP4)对子痫前期大鼠胎盘滋养层细胞的影响。方法构建子痫前期大鼠模型,采集正常孕鼠和模型大鼠胎盘滋养层组织,运用实时定量PCR和Western blot法检测CTRP4、白细胞介素1β(IL-1β)和caspase-1 mRNA和蛋白表达水平;分离培养正常孕鼠和模型鼠滋养层细胞,在不同时间点,运用流式细胞术检测碘化丙啶和caspase-1双阳性(PI+caspase-1+)细胞(pyroptosis),运用实时定量PCR和Western blot法检测IL-1β和caspase-1表达水平;在模型大鼠滋养层细胞培养基中分别加入(0.5、5、15、25、50)ng/m L CTRP4重组蛋白或(10、20)ng/m L CTRP4蛋白中和抗体,处理72 h后检测pyroptosis细胞数目和caspase-1、IL-1β水平。结果子痫前期大鼠胎盘滋养层组织caspase-1、IL-1β表达增强,CTRP4表达水平下调;CTRP4重组蛋白处理体外培养的大鼠滋养层细胞可显著减少PI+caspase-1+细胞数量并降低caspase-1、IL-1β水平,而CTRP4蛋白中和抗体处理显著增加PI+caspase-1+细胞数量并增强炎症反应。结论 CTRP4可显著抑制caspase-1/IL-1β炎症调节通路的活性,并抑制子娴前期大鼠胎盘滋养层细胞的pyroptosis。     

ICAM-1、P-选择素和D-二聚体在子痫前期中的相关性研究

目的：探讨子痫前期患者细胞间黏附分子-1(ICAM-1)、P-选择素(P-选择素)、D-二聚体(D-dimer)的水平变化及相互关系。方法：选择随机选取年龄、孕周、孕次相匹配的子痫前期孕妇90例为观察组,同期正常晚期妊娠孕妇92例为对照组,采用免疫组织化学SABC法检测两组研究对象胎盘组织中ICAM-1、P-选择素的表达水平;采用酶联免疫吸附ELISA法检测两组对象血浆ICAM-1、P-选择素和D-二聚体的表达水平。结果：子痫前期患者胎盘组织ICAM-1、P-选择素的表达水平明显高于正常对照组(P<0.05),在子痫前期组二者之间存在正相关性(r=0.523,P<0.05);两组孕妇血浆均有ICAM-1、P-选择素和D-二聚体的表达,子痫前期患者血浆ICAM-1、P-选择素和D-二聚体表达水平明显高于正常对照组(P<0.05),在子痫前期组三者之间相互呈明显正相关关系(分别为r=0.489, r=0.561和r=0.517,均P<0.05)。结论：子痫前期患者ICAM-1、P-选择素和D-二聚体的高表达可能与子痫前期的发生发展有关,监测这些指标对判断病情及指导治疗具有重要价值。     

香青兰总黄酮对子痫前期大鼠血管重构、内皮功能及胎盘组织中KLF14基因的影响

目的 研究香青兰总黄酮对子痫前期大鼠血管重构、内皮功能及胎盘组织中KLF14基因的影响。方法 6～8周龄雌性妊娠(妊娠第12天)SD大鼠55只,随机分为空白组(健康大鼠)、子痫组(子痫模型大鼠)、21 mg/kg组(模型+21 mg/kg组香青兰)、42 mg/kg组(模型+42 mg/kg组香青兰)、84 mg/kg组(模型+84 mg/kg组香青兰),每组11只。ELISA检测各组大鼠内皮功能相关指标;高分辨率小动物超声系统检测股动脉血流介导的FMD;H-E染色检测各组大鼠胎盘组织病理学形态;检测血管重构相关指标PWV;RT-PCR检测KLF14mRNA水平。结果 空白组大鼠胎盘完整;子痫组胎膜组织变薄,完整性差,有炎性细胞浸润,胎盘绒毛水肿、结构破坏、血管充血扩张。与子痫组相比,21 mg/kg组、42 mg/kg组、84 mg/kg组大鼠胎盘组织呈现不同程度的改善,且以高剂量组效果最为明显。空白组及香青兰总黄酮各剂量组FMD呈现先升高后下降的趋势,在2 min时达到峰值,子痫组FMD呈持续升高趋势,在5 min时达到峰值,时间与分组间有交互作用(P<0.05)。空白组及2...     

内皮型一氧化氮合酶运输介导物在子痫前期患者胎盘组织中的定位及定量研究

目的探讨内皮型一氧化氮合酶运输介导物(endothelial n itric oxide synthase traffic inducer,NOSTR IN)在子痫前期(pre-ec lampsia,PE)患者胎盘血管内皮细胞中表达的变化及其在子痫前期发病过程中的作用。方法HE染色后镜下观察胎盘组织及血管的病理变化,免疫组织化学方法及W estern b lot检测子痫前期患者胎盘组织中NOSTR IN的表达。结果HE染色显示子痫前期患者胎盘绒毛血管变细,数目减少,血管合体膜增厚,纤维素样坏死明显多于正常妊娠;免疫组织化学显示正常妊娠和子痫前期患者胎盘血管内皮细胞中都有NOSTR IN的表达,但子痫前期患者胎盘血管内皮细胞胞浆染色较正常妊娠明显增强;W estern b lot显示子痫前期患者胎盘组织中NOSTR IN的表达显著高于正常妊娠(P<0.01)。结论胎盘组织中NOSTR IN表达增加可能是子痫前期发病机制的重要环节之一。     

槲皮素对大鼠子痫前期模型血管内皮损伤及Nrf2/ARE信号通路的影响

目的 探讨槲皮素(QU)对子痫前期(PE)模型大鼠血管内皮损伤及核因子E2相关因子2(Nrf2)/抗氧化反应元件(ARE)信号通路的影响.方法 40只雌性大鼠与可育雄性大鼠交配,妊娠第0天(E0d)孕鼠分为对照组、QU组、脂多糖(LPS)组、QU+LPS组,每组10只.LPS组、QU+LPS组E0d开始输液泵尾静脉输入...     

子痫前期患者胎盘组织中visfatin蛋白与mRNA表达及意义

目的:探讨内脂素(visfatin,VF)在子痫前期(PE)患者胎盘组织中的表达及意义。方法:选择2011年8月至2013年12月在温州医科大学附属第一医院住院分娩的孕妇共计100例,根据病情轻重分为重度PE组、轻度PE组和正常妊娠组。采用苏木素-伊红染色法观察3组胎盘组织病理变化;免疫组化法及real-time PCR技术分别检测3组胎盘VF蛋白及mRNA的表达并分析其与子痫前期发病的关系。结果:PE的病理改变主要表现为细胞滋养细胞及合体滋养细胞结构紊乱且形态不完整;细胞滋养细胞增生,合体滋养细胞结节增多;绒毛毛细血管减少、淤血。免疫组化及real-time PCR结果显示胎盘组织中内脂素定位于合体及细胞滋养层细胞的胞浆,随着病情的加重,VF蛋白及mRNA表达量逐渐升高,重度PE组明显高于正常妊娠组,差异有统计学意义(P0.05)。结论:PE患者存在绒毛血管内皮细胞损伤和功能紊乱。胎盘VF蛋白及mRNA在PE孕妇中高表达,表明VF与PE的发生具有一定关系。     

桉叶油对维甲酸干扰大鼠胚胎植入及生长发育的影响

目的探讨桉叶油对维甲酸干扰大鼠胚胎植入及生长发育的影响。方法 SD孕鼠42只,随机分为6组,FA组正常对照组、溶剂组(花生油+RA)、3个实验组(桉叶油高、中、低剂量+RA)及RA组。溶剂组用花生油2ml/只于孕第7~14天灌胃,每天1次,孕第10天维甲酸40mg/kg灌胃1次。桉叶油3个剂量组分别用300mg/kg、200mg/kg、100mg/kg的桉叶油于孕第7~14天灌胃,每天1次,孕第10天维甲酸40mg/kg灌胃1次。RA组用40mg/kg的维甲酸于孕第10天灌胃1次。正常对照组给予自由摄食饮水。各组于孕21d早上处死孕鼠,取胚胎,记录孕鼠体重,子宫重,胎盘重。计胚胎植入总数,吸收胎数、活胎数、死胎数。观察胚胎外形,并测量胎鼠体重、身长、尾长。结果正常对照组、桉叶油+RA和溶剂+RA组孕鼠增重、子宫重、胎盘重与RA组比较均无差异;溶剂+RA组的孕鼠的胎盘重较其他各组低,与RA和桉叶油+RA各组比较差异无显著性,与正常对照组比较有差异(P0.05)。正常对照组的活胎率[(97.3±4.6)%]较灌胃维甲酸各组的活胎率高(P0.05),吸收胎率[(2.6±4.6)%]和畸形率(0)较灌胃维甲酸各组低(P0.05),死胎率为0;在灌胃维甲酸各组中,桉叶油高[(79.6±14.5)%]、中[(67.6±30.8)%]剂量组的活胎率较RA[(58.6±26.6)%]组高,但比较无差异;畸胎率[(44.5±41.6)%;(57.5±35.1)%]较RA[(68.1±43.6)%]组低,但差异无统计学意义。灌胃维甲酸各组的吸收胎率比较无差异。正常对照组的胎鼠体重、身长、尾长均值明显高于灌胃维甲酸各组胎鼠的体重、身长、尾长均值(P0.05);在灌胃维甲酸各组中,桉叶油各组胎鼠体重、身长的均值明显高于RA组和溶剂对照组(P0.05);溶剂对照组胎鼠体重、身长、尾长与RA组比较无差异;桉叶油各组胎鼠尾长的均值均高于RA组,但比较无差异。结论维甲酸干扰了大鼠胚胎的植入和发育,桉叶油对RA干扰大鼠胚胎植入有一定的拮抗作用,对RA引起的胎鼠生长发育迟缓有一定的抑制作用。     

单纯性肥胖大鼠的肥胖特点及瘦素的变化

目的:在单纯性肥胖大鼠中研究其肥胖特点及瘦素的变化。方法:60只新生SD大鼠随机分成两组,肥胖组(n=40)喂高能量饲料,对照组(n=20)喂普通饲料,动态观察体重、腹腔脂肪的变化,用免疫组化(ABC法)法观察腹腔脂肪细胞瘦素表达,用放免法测血清瘦素水平。结果:肥胖组大鼠与非肥胖对照组大鼠比,第7周体重增长最显,12周内体重持续上升,12周时腹腔脂肪重量增加,脂肪细胞增大,脂肪细胞瘦素表达增强,且与腹腔脂肪组织重量呈明显正相关,肥胖大鼠血清瘦素水平明显低于对照组(P＜0.05)。结论:在单纯性肥胖大鼠中体重、Lee's指数、腹腔脂肪重量、脂肪细胞大小变化显著。肥胖鼠的脂肪细胞瘦素表达增强,并与腹腔脂肪重量呈正相关,因此它可作为衡量大鼠肥胖程度的一项指标。     

Maternal protein restriction in the rat impairs resistance artery but not conduit artery function in pregnant offspring

Dietary protein restriction during gestation has been shown to produce vascular dysfunction in pregnant rats and hypertension in their offspring. However, no studies have to date examined the effects of such 'programming' on the vascular function of female offspring when they in turn become pregnant. We have therefore studied isolated conduit and resistance artery function from pregnant female offspring of control (C, 18 % casein) and protein-restricted (PR, 9 % casein) pregnant dams. There were no differences in birth weight, weight gain during pregnancy, litter size, fetal weight, placental weight, fetal : placental weight ratio or organ weights between the C and PR groups. In isolated mesenteric arteries, the vasodilatation in response to the endothelial-dependent vasodilator acetylcholine (ACh) and the β-adrenoceptor agonist isoprenaline was decreased in the PR group, while there were no differences in the constriction in response to potassium (125 m m ) or the α₁-adrenoceptor agonist phenylephrine (PE). No differences in any responses were seen in the isolated thoracic aorta. We conclude that dietary protein restriction in pregnancy programmes vasodilator dysfunction in isolated resistance arteries of female offspring when they become pregnant, but does not affect conduit arteries.     

健胎液对胎儿宫内发育迟缓孕鼠血浆、胎盘NO含量的影响

为从孕鼠血浆和胎盘一氧化氮（ＮＯ）水平探讨中药“健胎液”治疗胎儿宫内发育迟缓（ＩＵＧＲ）的机理，采用被动吸烟法建立ＩＵＧＲ动物模型，应用镀铜镉还原和内标比色法（Ｇｒｅｉｓ法），测定ＩＵＧＲ组、ＩＵＧＲ加健胎液组（用药组）孕鼠血浆及胎盘组织中ＮＯ的稳定代射终产物亚硝酸基／硝酸基（ＮＯ－２／ＮＯ－３）含量，并以正常孕鼠作对照。结果：与正常对照组和用药组相比，ＩＵＧＲ组胎鼠平均出生体重显著降低（Ｐ＜００１），ＩＵＧＲ组血浆及胎盘组织中ＮＯ－２／ＮＯ－３含量均显著降低（Ｐ＜００５～００１），而用药组和正常组相比，胎鼠平均出生体重、血浆及胎盘组织中ＮＯ－２／ＮＯ－３含量均无显著性差异（Ｐ＞００５）。结论：胎儿宫内发育迟缓的发生与ＮＯ的合成和释放显著降低，因而影响胎盘微循环，限制了母儿宫内发育迟缓。     

高压氧综合治疗胎儿宫内发育迟缓疗效观察

目的探讨在综合改善胎盘微循环的基础上,应用高压氧纠正胎儿宫内发育迟缓的疗效.方法将符合筛选指标的住院IUGR孕妇61例分为高压氧组28例(A组)和非高压氧组33例(B组),另外选择同期正常孕妇30例作为正常妊娠对照组(C组),比较B型超声、胎儿监护及新生儿结局等指标.结果1.高压氧综合治疗能显著降低PI、RI值,明显改善IUGR患者的脐血流;2.能明显促进胎儿生长,增加新生儿体重,提高IUGR的治愈率.结论高压氧结合常规治疗IUGR可获得较好临床疗效,值得临床推广.     

Increased adrenomedullin protein content and mRNA expression in human fetal membranes but not placental tissue in pre-eclampsia

The relationship between Pre-eclampsia (PE) and placental production of Adrenomedullin (AdM) is not completely understood. This study measured placental and fetal membrane AdM protein concentrations by specific radioimmunoassay and mRNA expression by Northern blot analysis in samples obtained at either term or preterm gestation from women either in labour or not in labour. Samples were obtained from women with normotensive and pre-eclamptic pregnancies. There were significant increases in immunoreactive AdM protein concentration (pg/mg DNA) in choriodecidua and amnion of women with PE compared to normal pregnancy for the preterm not-in-labour group (choriodecidua: control 124 +/- 16, n = 10, PE 361 +/- 35, n = 10; amnion: control 94 +/- 12, n = 10, PE 153 +/- 19, n = 10) and for the term not-in-labour (choriodecidua: control 128 +/- 17, n = 14, PE 459 +/- 51, n = 8; amnion: control 112 +/- 15, n = 14, PE 253 +/- 57, n = 8) and in-labour (choriodecidua: control 531 +/- 74, n = 14, PE 881 +/- 188, n = 8; amnion: control 545 +/- 84, n = 14, PE 1008 +/- 230, n = 8) groups. AdM mRNA relative abundance was greater in preterm, not-in-labour choriodecidual samples in PE, but not in amnion. In addition, this study observed labour-associated increases in choriodecidual and amniotic irAdM in term pre-eclamptic and control patients. However, there were no significant changes in AdM protein or mRNA expressions between any of the groups for placental tissue. These results suggest that fetal membranes, but not placental, production of AdM is increased at the post-translational level during PE in preterm and term tissues and at the pre-translational level during PE in preterm tissues. Fetal membranes, AdM may play an important role in the regulation of feto-placental hemodynamics and fetal physiology during pre-eclampsia.     

Down-regulation of placental transport of amino acids precedes the development of intrauterine growth restriction in rats fed a low protein diet

Intrauterine growth restriction (IUGR) represents an important risk factor for perinatal complications and for adult disease. IUGR is associated with a down-regulation of placental amino acid transporters; however, whether these changes are primary events directly contributing to IUGR or a secondary consequence is unknown. We investigated the time course of changes in placental and fetal growth, placental nutrient transport in vivo and the expression of placental nutrient transporters in pregnant rats subjected to protein malnutrition, a model for IUGR. Pregnant rats were given either a low protein (LP) diet ( n = 64) or an isocaloric control diet ( n = 66) throughout pregnancy. Maternal insulin, leptin and IGF-I levels decreased, whereas maternal amino acid concentrations increased moderately in response to the LP diet. Fetal and placental weights in the LP group were unaltered compared to control diet at gestational day (GD) 15, 18 and 19 but significantly reduced at GD 21. Placental system A transport activity was reduced at GD 19 and 21 in response to a low protein diet. Placental protein expression of SNAT2 was decreased at GD 21. In conclusion, placental amino acid transport is down-regulated prior to the development of IUGR, suggesting that these placental transport changes are a cause, rather than a consequence, of IUGR. Reduced maternal levels of insulin, leptin and IGF-1 may link maternal protein malnutrition to reduced fetal growth by down-regulation of key placental amino acid transporters.     

Placental and fetal development in straightbred and reciprocal crosses of Yorkshire and Ossabaw swine

Placental and fetal development were compared in 7 Yorkshire (Y) and 12 feral, Ossabaw (F) gilts mated to Y and F boars to produce straightbred and reciprocal cross litters (YY, YF, FY and FF, sire listed first). Gilts were slaughtered at d 75 +/- 2 of gestation. Ovulatory rate and litter size were higher in Y than in F gilts; however, rates of embyonal survival were similar in all groups. Groups differed in fetal body weight, metabolic body weight, crown-to-rump length, placental weight, metabolic placental weight and placental surface area, respectively. The YY group had highest values and the FF group smallest values for all variables except placental surface area. Pearson product-moment correlation coefficients of placental development with fetal length and weight across breeding groups were significant (e.g., placental surface area: fetal length, r = .67; placental surface area: fetal metabolic body weight, r = .76). It is concluded that the relationship between placental and fetal development observed in domestic swine is present in feral swine and crosses between domestic and feral swine at this gestational stage. These developmental measures are significantly influenced by fetal genotype and uterine environment but also by the breed of sire.     

4种肺动脉高压动物模型肺血管重构模式的差异研究

目的：探讨4种肺动脉高压（PH）动物模型肺血管重构模式的差异。方法:雄性SD大鼠（350-400g），分别通过腹主动脉-腔静脉分流（A-VF, n=10）、左肺切除（PE, n=10）、野百合碱注射（MCT, n=10）、左肺切除+MCT（PE+MCT,n=12）4种方法建立PH模型。检测平均肺动脉压力(mPAP）、RV/(LV+S)重量比值、肺小动脉中膜厚度百分比（WT%）、无肌性动脉肌化程度和新生内膜(neointima)形成、新生内膜增殖度和血管阻塞计分（VOS）。结果:在PE+MCT组（肺切除术后5周，MCT注射后4周）右肺腺泡内血管出现了新生内膜病变，其它组均没有新生内膜病变形成。PE+MCT组的动物出现了严重的右心室肥大，动脉中膜明显增厚，平均肺动脉压（mPAP）和无肌性血管肌化程度显著增加；A-VF、PE和MCT组仅形成轻-中度的右心室肥大、mPAP升高和小动脉肌化。结论:左肺切除联合应用MCT能成功诱导大鼠PH新生内膜模型，该模型能更好地模拟人类严重PH的病理改变，是研究梗阻性PH更为适用的动物模型。     

Igf2基因差异性甲基化区域在二(口恶)英致畸中的作用

目的研究2,3,7,8-四氯二苯并-对-二口恶英(2,3,7,8-tetrachlorodibenzo-p-dioxin,TCDD)对胎鼠生长发育的影响,探讨TCDD致畸与胰岛素样生长因子2(insulin-like growth factor2,Igf2)基因的表达和差异性甲基化区域(differentially methylated regions,DMRs)甲基化状态的关系。方法经灌胃给予孕10d大鼠10μg/kgTCDD,孕20天剖宫取胎,比较实验组和对照组孕鼠妊娠结局,测量两组活胎的顶臀长、体重和胎盘重;用实时定量-逆转录PCR检测孕20天胎鼠肝脏组织Igf2基因mRNA的表达;用蛋白印迹方法检测蛋白的表达水平;用甲基化限制酶HpaⅡ酶切-PCR法(HpaⅡ-PCR assay)检测两组胎鼠肝脏Igf2基因DMR1的甲基化程度,用亚硫酸氢盐测序方法检测Igf2基因DMR2的甲基化程度。结果对照组胎鼠均正常;实验组出现死胎及吸收胎,发生率为12.2%,畸形胎发生率为11.6%,活胎顶臀长、体重及胎盘重均明显低于对照组;对两组胎鼠肝脏组织Igf2基因表达的检测结果显示,实验组Igf2mRNA表达的相对量为0.77±0.11,对照组为0.27±0.15,两者差异有统计学意义(P<0.01);同时实验组肝脏组织Igf2蛋白的表达量也明显高于对照组;两组胎鼠肝脏Igf2基因DMR1的甲基化程度无差异,DMR2甲基化程度实验组明显低于对照组。结论孕期暴露于TCDD可导致大鼠发生死胎、吸收胎、畸形胎和胎儿宫内发育迟缓,TCDD所致胎鼠发育异常可能与胎鼠肝脏组织Igf2基因DMR2甲基化程度降低引起的Igf2高表达有关。     

母体肢体缺血预处理对宫内窘迫胎鼠复氧后海马神经元凋亡的影响*

 目的： 观察母体的肢体缺血预处理(LIP)对宫内窘迫胎鼠复氧后海马神经元凋亡的影响。方法: 采用微动脉夹阻断母鼠通向子宫和卵巢的动静脉15 min后开放以制备胎鼠宫内窘迫模型。孕19 d SD大鼠12只,随机分为4组：空白对照（S）组、LIP组、胎儿窘迫（FD）组和LIP+FD组。各组母鼠再灌注2 d时剖宫取活胎鼠12只断头取脑。TUNEL法测定胎鼠海马CA1区神经元凋亡情况,计算细胞凋亡指数;免疫组化法和Western blotting法测定Bcl-2和Bax蛋白的表达。结果: 与S组比较,FD组和LIP+FD组胎鼠海马CA1区神经元凋亡指数增加（P＜0.05）,Bcl-2蛋白表达增加,Bax蛋白表达增加,Bcl-2/Bax比值降低;与S组比较,LIP组胎鼠海马CA1的 Bcl-2、Bax蛋白表达及Bcl-2/Bax蛋白表达的比值无明显改变（P＞0.05）;与FD组比较,LIP+FD组细胞凋亡指数降低（P＜0.05）,Bcl-2/Bax比值增加。结论: 母体肢体缺血预处理减轻了宫内窘迫胎鼠复氧后海马神经元的凋亡,其机制可能与Bcl-2蛋白表达的上调相关。