边缘型维生素A缺乏对幼鼠学习记忆的影响及干预效果

目的了解胚胎期开始的边缘型维生素A缺乏(MVAD)对幼鼠学习记忆的损害及幼年期干预的效果。方法实验分为正常对照组、边缘型维生素A缺乏组(MVAD组)、维生素A干预组(VAI组)。正常对照组(幼鼠10只)母鼠和幼鼠均给予VA充足饲料;MVAD组(幼鼠19只)母鼠和幼鼠均给予边缘型维生素A缺乏饲料;VAI组(幼鼠9只)母鼠给予边缘型维生素A缺乏饲料,幼鼠于生后4周开始给予VA充足饲料。待各组幼鼠长至7周龄,用穿梭箱主动回避反应实验测试学习记忆功能,离体脑片检测海马长时程增强(LTP),激光共聚焦检测脑片强直刺激后细胞内钙离子浓度的变化。结果(1)穿梭箱主动回避反应实验达到学会标准的训练次数:VAI组(28.8±4.1)次和MVAD组(45.6±12.1)次分别多于正常对照组(17.1±4.4)次(P<0.01),MVAD组的训练次数多于VAI组(P<0.05);(2)海马脑片诱发LTP的场兴奋性突触后电位(fEPSP)斜率增加的百分比:MVAD组(22.9±9.4)%和VAI组(29.5±13.7)%小于正常对照组(57.5±27.3)%(P<0.01),VAI组与MVAD组差异无统计学意义;(3)激光共聚焦检测脑片强直刺激后细胞内相对荧光强度:MVAD组(65.1±17.0)和VAI组(85.8±17.1)低于正常对照组(113.6±20.5)(P<0.01),MVAD组低于VAI组(P<0.05)。结论胎儿期开始的MVAD可导致幼鼠学习记忆功能和海马LTP受损,生后4周给予VA干预,其学习记忆功能有部分恢复;VA可以通过调节细胞钙离子内流而影响LTP。     

轻度维生素A缺乏对大鼠肺发育中肺组织血小板源性生长因子A表达的影响

目的 观察轻度维生素A缺乏(MVAD)对大鼠肺发育中血小板源性生长因子A(PDGF-A)表达的影响.方法 32只清洁级SD大鼠,雌雄各半.雌鼠随机分为MVAD组(n＝10)和对照组(n＝6).MVAD组喂养维生索A(VitA)缺乏饲料,对照组喂养正常饲料.3周后雌雄鼠交配,建立MVAD孕鼠模型.高效液相色谱法检测2组雌鼠血清VitA水平和孕20d胎鼠肝脏VitA水平;测量出生1d乳鼠身长、尾长、体质量;取MVAD组和对照组出生1d乳鼠肺组织,反转录(RT)-PCR方法检测出生1d乳鼠肺脏PDGF-A mRNA的表达,免疫组织化学方法检测其PDGF-A蛋白的表达水平.应用SPSS 13.0软件进行统计学分析.结果 MVAD组雌鼠毛色干枯,少食少动,孕鼠部分流产不孕.MVAD组雌鼠血清VitA水平显著低于对照组(P＜0.05).MVAD组孕20d胎鼠肝脏VitA水平亦显低于对照组(P＜0.05).MVAD组出生1d乳鼠身高、尾长及体质量数值均低于对照组(P,＜0.05).MVAD组出生1d乳鼠肺组织PDGF-A mRNA表达量显著低于对照组(P＜0.05);免疫组织化学检测出生1d乳鼠肺组织支气管上皮细胞、肺泡上皮细胞、血管内皮细胞内均可见PDGF-A蛋白表达,MVAD组PDGF-A蛋白表达量较对照组少(P＜0.05).结论 VitA在肺发育中起重要作用,MVAD引起PDGF-A的表达减少,可能是大鼠肺发育障碍的原因之一.     

新生儿边缘型维生素A缺乏临床分析

目的分析新生儿与孕妇妊娠晚期维生素A(VA)水平是否具有相关性,对比不同喂养方式的新生儿VA水平状况,探讨边缘型VA缺乏(MVAD)的治疗效果。方法分析2015年5月至2017年5月在沈阳医学院附属中心医院均接受静脉采血行VA检查的妊娠晚期孕妇与新生儿病例各357例,其中MVAD的新生儿251例,VA水平正常的新生儿106例,分析不同喂养方式下MVAD的发病率,随访观察不同喂养方式下MVAD的有效率。结果 (1)妊娠晚期孕妇与新生儿的VA水平具有相关性(r=0.307,P0.01);(2)MVAD新生儿生后1.5个月母乳喂养组中母子同服者治疗有效率为93.75%,人工喂养组为83.33%,单一新生儿给药者为66.67%。(3)血清VA水平正常的新生儿(未干预)生后1.5个月母乳喂养新生儿MVAD发病率为67.34%;人工喂养为33.33%,混合喂养为36.36%,母乳喂养的发病率高于人工喂养,差异具有统计学意义(P0.05)。(4)给予VA口服干预治疗,生后4.5个月总体MVAD发病率明显下降(χ2=9.353,P0.002)。结论新生儿MVAD与妊娠晚期孕妇VA水平密切相关,VA的检测应作为孕妇和新生儿的常规检查;母乳喂养的新生儿MVAD的发病率较高,应作为重点干预对象;尽早给予VA口服可提高MVAD的治疗有效率,降低发病率。     

轻度维生素A缺乏对不同时期胎鼠肺发育的形态学影响

目的 观察轻度维生素A缺乏(MVAD)对不同时期胎鼠肺发育的形态学影响.方法 24只SD雌鼠随机分为MVAD组(n=15)和对照组(n=9).通过喂养缺乏维生素A(VA)饲料建立MVAD孕鼠模型,高效液相色谱法检测2组雌鼠血清VA水平和孕20 d胎鼠肝脏VA水平.取孕16 d、20 d、出生1 d MVAD组和对照组胎(乳)鼠肺组织,经HE染色,光镜下观察其肺形态学改变,比较MVAD组和对照组鼠血清VA、孕20 d肝VA水平及胎肺发育的形念学区别.应用SPSS 13.0软件进行统计学分析.结果 MVAD组雌鼠毛色干枯,少食少动,孕鼠体质量下降,部分流产不孕,平均孕胎数较对照组下降(P＜0.05);出生1 d MVAD组乳鼠体质世、身长、尾长值均较对照组小(Pa＜0.01).MVAD组雌鼠血清VA水平显著低于对照组(P＜0.01),孕20 d胎鼠肝脏VA水平MVAD组亦显著低于对照组(P＜0.01).HE染色显示MVAD组16 d胎鼠支气管圆形管腔较对照组分支样管腔幼稚;MVAD组20 d胎鼠较埘照组原始肺泡少,平均肺泡表面积较小,肺泡间隔较厚(P＜0.01);MVAD组出生1 d乳鼠表现为肺发育的不均一性,较多区域有肺泡过度膨胀,肺泡间隔较薄(P＜0.01),有离断;局部又有肺泡膨胀小全,间质充血,肺泡间隔增厚.结论 VA在肺发育中起重要作用,MVAD会导致胎鼠肺发育小全.     

芪归合剂促进肾病综合征鼠肝IGF-Ⅰ、IGFBP-3表达的研究

目的观察芪归合剂对肾病综合征鼠(NS鼠)胰岛素样生长因子-Ⅰ(IGF-Ⅰ)、胰岛素样生长因子结合蛋白-3(IGFBP-3)的作用.方法制备大鼠阿霉素NS模型,设正常对照组、NS组、NS蒸馏水治疗组和NS芪归合剂治疗组,每组5只大鼠.以放射免疫法和免疫放射法测定各组血、尿IGF-Ⅰ和IGFBP-3水平;用RT-PCR法检测肝IGF-ⅠmRNA、IGFBP-3mRNA表达;测量鼠的身长、体重和血生化指标.结果NS组鼠体重增长[(47±34)g/4周]、身长增长[(2.6±0.8)cm/4周]、血IGF-Ⅰ[(491±66)μg/L]、IGFBP-3[(102±4)μg/L]低于正常鼠组[分别为(162±19)g/4周、(8.1±1.5)cm/4周、(968±184)μg/L、(133±16)μg/L],尿IGF-Ⅰ[(264±119)ng/24h]高于正常鼠组[(59±16)ng/24h],而肝IGF-ⅠmRNA表达(0.52±0.04)与正常对照组(0.53±0.06)相似、IGFBP-3mRNA表达(0.56±0.05)低于正常鼠组(0.93±0.05).芪归合剂治疗组肝IGF-ⅠmRNA表达(0.93±0.05)、IGFBP-3mRNA表达(0.87±0.05)高于NS蒸馏水治疗组.结论NS鼠存在IGF-Ⅰ、IGFBP-3代谢紊乱和生长障碍,血IGF-Ⅰ降低主要是由于尿中排出所致,而血IGFBP-3降低主要与合成减少有关.芪归合剂能增加NS鼠肝IGF-ⅠmRNA、IGFBP-3mRNA表达.     

哮喘大鼠信息传递与转录活化因子6的表达和地塞米松对其表达的影响

目的研究哮喘大鼠支气管信息传递与转录活化因子6(STAT6)的表达和地塞米松(DXM)对其表达的影响。方法30只体重120～180g的二级幼年雄性SD大鼠,随机分为3组:正常对照组(A组)、哮喘组(B组)、地塞米松组(DXM组)。对支气管肺泡灌洗液(BALF)进行细胞总数、嗜酸性粒细胞(EOS)计数和分类计数;应用双抗体夹心酶联免疫吸附试验法测定BALF和血清中白细胞介素4(IL4)浓度;采用免疫组化法和原位杂交法分别检测支气管STAT6蛋白和STAT6mRNA的表达。结果(1)B组支气管STAT6蛋白和STAT6mRNA表达[(0.171±0.025),(0.180±0.013)]均高于A组[(0.082±0.022),(0.091±0.012)]和DXM组[(0.114±0.013),(0.114±0.010)](均为P<0.01),其主要表达细胞是上皮细胞;(2)支气管STAT6蛋白、STAT6mRNA分别与BALF中的IL4浓度呈显著正相关(r=0.664、0.785,P<0.01),STAT6蛋白、STAT6mRNA分别与BALF中的EOS绝对值呈显著正相关(r=0.869、0.884,P<0.01)。结论哮喘大鼠支气管有STAT6的较强表达,上皮细胞是其主要表达细胞;地塞米松可以下调STAT6的表达,可能为其抑制哮喘气道炎症形成的重要作用机制。     

母鼠孕期补充α-亚麻酸或二十二碳六烯酸对其幼鼠脂质代谢的影响

目的了解母鼠孕期补充α-亚麻酸(LNA)或二十二碳六烯酸(DHA)对其新生幼鼠脂质代谢的影响。方法实验母鼠24只,随机分为三组,在母鼠孕期分别给予不同饲料喂养:对照组母鼠给予普通饲料;LNA组给予补充LNA(100mg/d);DHA组给予补充DHA(100mg/d)。三组母鼠分娩后,分别将其幼鼠杀死取血,测定各组幼鼠血浆中脂肪酸的含量,并与母鼠血中脂肪酸含量进行比较。结果母鼠孕期补充DHA组其幼鼠血浆中DHA的含量显著高于对照组和补充LNA组幼鼠;孕期补充LNA组其幼鼠血浆中LNA含量明显升高,血浆中DHA的含量也明显高于对照组;母鼠血中DHA和LNA的含量与其幼鼠血中DHA和LNA的含量显著相关(r=0.813、0.883,P均<0.01)。母鼠孕期补充DHA其幼鼠血浆中花生四烯酸(AA)的含量低于对照组和LNA组幼鼠。结论母鼠孕期补充DHA后可明显提高其新生幼鼠血中DHA的含量;母鼠孕期补充LNA后其新生幼鼠血中DHA含量也有升高,但升高程度没有补充DHA组显著;孕期补充DHA对婴儿脑和视网膜的发育有帮助,但补充DHA或LNA时应注意适当的剂量。     

大剂量甲泼尼龙对婴儿痉挛幼鼠脑组织的保护作用

目的 婴儿痉挛症(infantile spasms,IS)是婴儿期最常见的难治性癫痫性脑病,但相关动物实验缺乏,该研究通过构建IS动物模型,探讨大剂量甲泼尼龙对IS幼鼠脑组织的影响.方法 将生后10 d(P10)SD大鼠随机分为对照组、模型Ⅰ组和模型Ⅱ组,每组30只.模型Ⅰ组和模型Ⅱ组分别在P10、P13腹腔注射N-甲基-D-天冬氨酸(N-methyl-D-aspartate,NMDA)诱发癫痫发作,模型Ⅱ组在P13应用NM-DA前连用3 d甲泼尼龙.观察幼鼠癫痫发作并评分,原位末端标记法(TUNEL)检测凋亡情况,免疫组织化学法测Bax、Bcl-2蛋白表达、实时荧光定量PCR检测海马组织Bcl-2、Bax和caspase-3 mRNA的表达.结果 (1)P13模型Ⅰ组癫痫发作率83.3%(25/30),模型Ⅱ组均未出现发作,模型Ⅱ组较模型Ⅰ组癫痫发作率明显降低;(2)模型Ⅱ组凋亡细胞数(14.37±2.02)少于模型Ⅰ组(25.67±1.52),多于对照组(9.00±2.50),差异均有统计学意义(均P<0.05);(3)模型Ⅱ组Bax蛋白及mRNA表达量(44.55±3.58,2.35±1.01)明显低于模型Ⅰ组(58.05±4.62,3.27±0.95),高于对照组(28.90±5.14,1.68±0.50),差异均有统计学意义(均P<0.05);(4)模型Ⅱ组caspase-3mRNA表达量(5.99±1.75)低于模型Ⅰ组(7.88±1.60),高于对照组(3.60±1.70),差异均有统计学意义(均P<0.05).结论 大剂量甲泼尼龙能减轻NMDA致IS幼鼠癫痫发作;大剂量甲泼尼龙对NMDA致IS幼鼠具有脑保护作用,这种保护作用可能与其减轻癫痫发作,减少细胞凋亡有关.     

Foxp3基因表达与CD4+CD25+调节性T细胞在急性特发性血小板减少性紫癜发病中的作用

目的 研究Foxp3基因与CD4+CD25+调节性T细胞(Tr细胞)在急性特发性血小板减少性紫癜(AITP)患儿中的表达变化,探讨其在AITP发病机制中的作用.方法 流式细胞仪分别检测AITP患儿和正常健康儿童外周血Tr细胞的数量,酶联免疫吸附法(ELISA)检测其外周血IL-10、TGF-β水平,RT-PCR检测外周血单个核细胞中转录因子Foxp3 mRNA的表达.结果 AITP患儿外周血Tr细胞的数量明显低于正常对照组[(2.83±1.05)% vs (5.07±0.59)%,P＜0.05].相关细胞因子中IL-10、TGF-β水平也明显低于正常对照,[IL-10(29.48±13.69) vs (43.10±14.95) ng/L ;TGF-β1(170.04±91.58) vs (254.75±130.41) ng/L,Pa＜0.05].与对照组比较,AITP患儿外周血单个核细胞中转录因子Foxp3 mRNA水平明显降低[(0.74±0.14)% vs (0.34±0.12)%],差异有统计学意义(P＜0.05).结论 AITP患儿中Tr细胞数量的减少,相关细胞因子水平减低,Foxp3 mRNA表达降低,可能在AITP发病中起重要作用.     

巨噬细胞炎性蛋白1α及其mRNA在哮喘小鼠气道炎症中的作用

目的探讨巨噬细胞炎性蛋白1α(MIP-1α)及其mRNA在哮喘小鼠气道炎症中的作用.方法 70只二级雄性BALB/C小鼠随机分为2大组7小组(1)正常小鼠组,分成灌洗组(A24组)和未灌洗组(A0组);(2)哮喘小鼠组,分成灌洗组(根据末次激发时相不同分成B3组、B8组、B24组和B36组)和未灌洗组(B0组).对支气管肺泡灌洗液(BALF)进行嗜酸性粒细胞(EOS)计数和分类计数;应用双抗体夹心酶联免疫吸附试验法测定血清和BALF中MIP-1α的浓度;采用免疫组化法和原位杂交法检测MIP-1α蛋白和MIP-1α mRNA的表达.结果 (1)BALF和血清中MIP-1α的浓度B3组[(30.2±4.2)pg/ml,(30.8±4.6)pg/ml]、B8组[(35.3±4.9)pg/ml,(34.9±5.1)pg/ml]、B24组[(42.9±5.8)pg/ml,(41.7±6.3)pg/ml]和B36组[(37.8±4.7)pg/ml,(35.7±4.9)pg/ml]均高于A24组[(20.9±3.8)pg/ml,(22.4±4.3)pg/ml](P均<0.01); MIP-1α浓度3 h开始升高,24 h达峰值,36 h已下降;(2)免疫组化和原位杂交显示,B0组支气管MIP-1α蛋白和MIP-1α mRNA的阳性表达率[(26.4±6.2)%, (23.9±4.2)%]均高于A0组[(10.3±2.5)%, (8.7±1.8)%](P均<0.01),其表达的主要细胞是上皮细胞;(3)哮喘小鼠BALF中MIP-1α的浓度和EOS绝对值之间呈显著正相关(r=0.890, P＜0.01),MIP-1α的浓度和EOS占细胞总数百分比(EOS %)之间呈显著正相关(r=0.897, P＜0.01).结论哮喘小鼠MIP-1α蛋白和mRNA较强表达,上皮细胞是主要表达细胞,MIP-1α动力学特点为3 h开始升高,24 h达峰值,36 h已下降,并与EOS聚集密切相关.     

Vitamin D deficiency, pancreatic and small intestinal enzyme development in rats

Maternal vitamin D deficiency has been shown to lead to reduced body weights in developing rat pups. To evaluate the effects of vitamin D deficiency alone both in dams and pups during the perinatal age on the ontogeny of gastrointestinal enzymes, female weanling rats (3 weeks of age) were divided into three groups. Groups I and II were fed a control (vitamin-D-replete) diet. Group II were fed a vitamin-D-deficient diet. Six weeks afterward they were mated with normal male rats while continuing on their respective diets until sacrifice. Only rats that delivered their pups on the same day from each group were brought into the study. Litter sizes of groups I and II were adjusted to 10, while group III was adjusted to 13 such that the rate of growth paralleled that of group II. At 19 days after birth, all dams and pups were sacrificed. There were no differences in the calcium and phosphorus contents in breast milk obtained from dams of each group. The serum calcium concentration of pups from group II (vitamin-D-deficient) was lower than the other groups. Body weights of pups from groups II and III were significantly lower than those of group I. The mucosal weight, total mucosal protein, mucosal DNA, sucrase, and maltase activities from groups II and III were similar, but lower than group I. Pancreatic weight, total pancreatic protein, DNA, amylase, and lipase activities from groups II and III were also similar, but lower than group I. Vitamin D deficiency was confirmed in both dams and pups from group II.(ABSTRACT TRUNCATED AT 250 WORDS)     

Ontogenic changes in serum immunoglobulins and C3 in vitamin-D deficient and malnourished rats

In both protein energy malnutrition and vitamin D deficiency, defects in some immunological functions have been noted, but the effects on complement and immunoglobulin concentrations have not been evaluated. We assessed the effects of malnutrition and vitamin D deficiency on immunoglobulins and C3 in rats in early postnatal life during weaning and early adulthood using the rocket immunoelectrophoresis technique. In well-nourished rats, the serum levels of IgG increased from 88.5 +/- 10.2 mg/dl in the newborn period to 883.4 +/- 104.8 mg/dl at weaning (day 19). The adult levels, 1,325.9 +/- 60.8 mg/dl, were attained by 35 days of age. Serum IgA was not detectable by our method until 20 days of age (1.1 +/- 0.2 mg/dl) and reached adult levels (13.4 +/- 3.2 mg/dl) by day 35. IgM was detectable in the serum of pups at 5 days of age (0.4 +/- 0.07 mg/dl), increased to 27.5 +/- 6.9 mg/dl at weaning and approached adult levels (93.7 +/- 9.9 mg/dl) at day 35. C3 levels at birth were only 36% of adult levels and did not change during the suckling period. They then increased to levels comparable to those of adults at the age of 35 days. Serum immunoglobulins and C3 in malnourished rats were not significantly different from age-matched control pups. In pups born to dams fed a vitamin-D-deficient diet from 3 weeks of age, only the serum IgG and C3 levels were significantly lower than those of normal pups at day 1 (IgG level: 65.2 +/- 6.1 vs. 88.5 +/- 10.2 mg/dl; C3 level: 20.3 +/- 6.9 vs. 36.2 +/- 3.1% of an adult level; p less than 0.005). Thus the increased susceptibility of malnourished young animals to infection does not appear to be related to a lowering of serum immunoglobulin and complement concentrations.     

Effects of dietary choline and N,N-dimethylaminoethanol on lung phospholipid and surfactant of newborn rats.

Pups delivered by rats fed during pregnancy a choline-deficient (CD) diet containing 1% N,N-dimethylaminoethanol (DME) die within 36 hr of birth. The concentrations of sphingomyelins, phosphatidyl cholines, and disaturated phosphatidyl cholines in the lungs of these pups are lower than those in the lungs of pups delivered by dams fed a choline-supplemented diet (CS). The amount of surfactant isolated from the lung of the pups was also reduced. These changes were accompanied by alterations in the activity of enzymes (choline kinase, EC 2.7.1.32; choline phosphotransferase, EC 2.7.8.2) involved in the synthesis of lung lecithins. These results strongly suggest that pups delivered by dams fed a CD diet containg 1% DME die of respiratory distress syndrome due to altered metabolism of lung surfactant.     

宫内生长迟缓大鼠脂肪组织肿瘤坏死因子αmRNA表达与胰岛素抵抗关系的研究

目的探讨内脏脂肪组织肿瘤坏死因子α(TNF-α)的mRNA表达与宫内生长迟缓(IUGR)大鼠成年后胰岛素抵抗(IR)发生的关系,以及生后早期不同的营养模式的远期影响.方法用母鼠全程饥饿法建立IUGR动物模型.32只IUGR新生雌鼠随机分为4组IUGR模型组(S/N组)给予常规饮食,IUGR高热能饮食组(A组),IUGR高蛋白高热能饮食组(B组),IUGR高蛋白质等热能饮食组(C组).各组幼鼠在3周哺乳期间母鼠分别摄取上述饲料.第4周起各组幼鼠断乳后全部改为自由进食常规饮食至实验结束.另以正常母鼠所生正常新生雌鼠8只为正常对照组(C/N组)生后给予常规饮食喂养至实验结束.各组大鼠在48周(中老年期)时分别测定体重、肾周脂肪重量、脂肪组织TNF-αmRNA表达,计算ISI(胰岛素敏感指数)并分析其与TNF-αmRNA表达量及肾周脂重、脂重/体重的相关性.结果IUGR模型组及IUGRA、B组胰岛素敏感性下降,并且脂肪组织TNF-αmRNA表达及肾周脂重、脂重/体重显著高于正常对照组(P<0.05或0.01);IUGR的C组胰岛素敏感性及TNF-αmRNA表达量、脂重/体重与正常对照组差异无统计学意义(P>0.05).脂肪组织TNF-αmRNA水平与肾周脂肪重量、脂重/体重量呈正相关,与ISI呈负相关.脂重/体重与ISI呈负相关.结论IUGR大鼠成年后发生胰岛素抵抗可能经由中心性肥胖的途径,与腹脂增多、脂肪细胞过度表达TNF-α有关,脂源性TNF-α可能是IUGR胰岛素抵抗的重要协病因素.高蛋白的早期营养模式可能通过实现IUGR个体的骨骼肌的生长追赶而非脂肪追赶避免了中心性肥胖和胰岛素抵抗的发生,是较合理的早期营养饮食模式.     

Caffeine decreases zinc and metallothionein levels in heart of newborn and adult rats.

The purpose of the present study is to show that dietary caffeine, heart tissue Zn levels, and metallothionein (MT) concentration are all interrelated in newborn rats. Dams with eight pups in the control group were fed a 20% protein diet upon delivery, whereas dams in the experimental group were fed a 20% protein diet supplemented with caffeine (2 mg/100 g body weight). Offspring were killed at d 22 postbirth and the hearts and livers were removed to determine the Zn and MT concentrations. Hearts of the newborn rats in the caffeine group showed decreased Zn levels as well as decreased MT concentration. To explain the observed effects in newborn rats, the relationship between Zn and MT levels was studied in adult female rats. They were injected intraperitoneally with either ZnCl2 (20 mg/kg body weight) dissolved in saline solution or ZnCl2 and caffeine (4 mg/kg body weight) over a period of 2 d. Injection of ZnCl2 into adult female rats resulted in an increase in heart MT levels, whereas injection of caffeine caused decreased Zn levels and MT concentration. Current findings indicate that dietary caffeine intake during the lactational period by newborn pups causes a decrease of the heart Zn and MT levels.     

Body weight and brown fat activity in hyperphagic cafeteria-fed female rats and their offspring

Presenting pregnant rats with a varied choice of human food items (a cafeteria diet) caused a slight reduction in total protein intake and significant increases in energy intake (32%) and weight gain compared to pregnant females fed stock diet (controls). Cafeteria-fed mothers gave birth to the same number and weight of pups as controls, and these grew normally, but were fatter at weaning than control pups. Cafeteria-fed dams lost more weight than controls during lactation, in spite of sustained hyperphagia, and body fat and energy was the same as controls at 21 days post-partum. Brown adipose tissue protein content and thermogenic activity (assessed from mitochondrial purine nucleotide binding) were both elevated in cafeteria-fed mothers when compared to controls at 21 days post-partum, but brown fat activity in their offspring at weaning did not differ between treatments, although tissue protein content was depressed in the pups of cafeteria-fed dams.     

孕鼠维生素A缺乏对子代鼠肾发育及肿瘤发生的影响

目的 建立维生素A缺乏的孕鼠模型,观察孕鼠维生素A缺乏对子代鼠胚胎发育和肿瘤发生的作用.方法 取Wismr雌鼠9只,12周龄,体重200～220g.将其分成2组:①维生素A缺乏饮食组6只,受孕前2周起无维生素A饮食直至产后;②正常对照组3只,给予正常饮食.所有雌鼠喂养2周后与健康Wistar公鼠交配成孕鼠.二组孕鼠产后均给予正常饮食,于哺乳期结束后立即处死.分娩后第二天每组分别随机抽取15只新生子代鼠立即处死.其余子代鼠生后给予正常饮食,至生后365 d处死、解剖(如发现中途死亡,即刻解剖).观察二组大鼠产子情况、新生子代鼠血清维生素A浓度、新生子代鼠肾发育形态、子代鼠肿瘤发生率和组织中RXRαmRNA表达.结果 维生素A缺乏饮食组孕鼠产子代鼠51只;正常对照组孕鼠产子代鼠44只.维生素A缺乏饮食组的新生子代鼠血清维生素A浓度为(0.51±0.13)μmol/L,明显低于对照组的新生子代鼠的血清维生素A浓度(0.81±0.15)μmol/L,P=0.000.二组新生子代鼠中均未发现肿瘤组织,但维生素A缺乏饮食组的新生鼠组织中未成熟的肾小球和肾小管较对照组多见.维生素A缺乏组的新生子代鼠双肾中肾源性剩余检出率为60.0%,明显高于对照组(26.7%,P=0.018).维生素A缺乏饮食组子代鼠36只,1只中途死亡,肾母细胞瘤发生率13.9%.对照组的子代鼠无肿瘤发生.维生素A缺乏饮食组子代鼠肾源性剩余检出率30.6%,明显高于对照组子代鼠肾源性剩余检出率(6.9%,P=0.001).子代鼠中肾母细胞瘤组织的RXRαmRNA表达强度为(3.17±0.15),明显低于对照组肾脏组织中RXRαmRNA表达强度(3.58±0.20),P=0.000.结论 大鼠孕期维生素A缺乏会导致子代鼠肾发育差,肾源性剩余增加,肾母细胞瘤发生率增高.维生素A可能通过上调RXRαmRNA的表达来促进肾脏分化和降低肿瘤发生.