营养

042 70 5　大鼠缺锌时股骨骺生长板的病理形态学改变/张月红…∥卫生研究 2 0 0 3 ,3 2 (1 ) 1 6～ 1 9为观察大鼠缺锌时股骨骺生长板的病理形态学改变 ,将 3 0只Wistar大鼠按体重随机分为 3组 :缺锌组 ,对照组和对喂组 ,每组动物 1 0只。缺锌组和对照组饲料锌含量分别为 3 9和 2 4 7mg/kg ,对喂组饲对照组饲料 ,饲料摄入量与缺锌组相同。动物喂养 8周后处死 ,在普通光学显微镜下观察大鼠股骨组织病理变化并运用形态计量学方法定量描述 ,测定血清骨钙素和生长激素含量。结果发现缺锌组大鼠股骨骺生长板软骨细胞畸形、数量减少 ,骺端骨…     

缺锌对生长期大鼠骨形态计量学参数的影响

目的　研究缺锌对生长期大鼠股骨远端骨干骨形态计量学参数的影响 ,阐明锌与骨骼发育的关系 ,为生长发育期儿童合理补充锌提供科学依据。方法　 3 0只 Wistar大鼠 ,雌雄各半 ,体重 (1 0 0± 2 0 ) g,按体重随机分为三组 ,每组 1 0只 ,缺锌组和对照组饲料锌含量分别为 3 .9和2 4 .7mg/kg,对喂组喂对照组饲料 ,饲料摄入量与缺锌组相同。动物喂养 8w后处死 ,用骨形态计量学方法研究缺锌对大鼠骨组织形态学和动态学参数的影响。结果　与对照组和对喂组相比 ,缺锌组骨小梁体积显著减少、骨小梁板密度降低而间隙明显增大、骨小梁个数减少、骨形成速度降低、类骨质表面积显著减少、骨基质成熟时间明显延长、矿化沉积速率降低、矿化延迟时间增加 ,且均有显著性差异 (P<0 .0 5 )。结论　缺锌可明显降低骨形成 ,延迟骨矿化 ,破坏骨的空间结构 ,并使骨小梁连接性减弱 ,离散程度增加。     

生长期大鼠缺锌时股骨病理形态学的改变

目的　通过建立生长期缺锌大鼠模型以阐明锌缺乏对生长期儿童骨骼发育的影响 ,为儿童生长发育迟缓的防治提供理论依据。方法　刚断奶的雄性大鼠随机分为对照组 (ZA)、缺锌组 (ZD)、配饲组 (PF) 3组 ,每组 10只。喂养 15天后处死 ,取股骨称量重量及测量长度、直径 ,并做病理组织切片 ,观察股骨病理改变。结果　ZD组股骨长度 [(2 4 . 80± 0 . 4 2 )mm]明显低于PF组 [(2 6 . 70± 0 . 4 8)mm]及ZA组 [(2 7. 90± 0 . 32 )mm](P <0 . 0 1) ;ZD组股骨直径 [(2 . 0 9± 0 .0 9)mm]明显低于PF组 [(2 . 70± 0 . 0 8)mm]及ZA组 [(2 . 80± 0 . 0 8)mm](P <0 . 0 1) ;ZD组股骨重量 [(0 .5 1± 0 . 0 5 )g]明显低于PF组 [(0 . 6 5± 0 . 0 8) ]及ZA组 [(0 . 76± 0 . 10 )g](P<0 . 0 1)。缺锌组大鼠股骨骺生长板软骨细胞畸形、数量减少 ,骺端骨小梁纤细、疏松、排列紊乱、髓腔相对扩大 ,骨小梁体积显著减少 ,骨小梁板密度降低 ,骨小梁间隙增大。结论　生长期动物缺锌可导致骨骼的形态及病理发生改变而影响骨骼的生长发育。     

对长期低钙摄入幼鼠骨骼的研究——Ⅱ低钙时幼鼠股骨生长板的病理变化

本文研究在VitD营养正常有不同程度低钙时对生长着幼鼠股骨生长板的生长、骨矿化、骨组织学的变化。实验采用21～23日龄Wistar断乳雄鼠45只。随机分为3组:A组,对照组,饲料含钙0.5％;B组,中度低钙(0.15％);C组,重度缺钙(0.03％)。于实验中期(3周)、末期(6周)分别处死1/2幼鼠,取左后肢股骨制成病理切片(4μm)。光镜下观察结果示B组中度低钙幼鼠股骨干骺端生长盘软骨显著厚于A组,尤以增生区和基质钙化区著;空泡细胞层显著增加6～14层(正常约4～5层);骨小梁粗乱;成骨细胞增生。C组重度缺钙幼鼠股骨干骺端生长板软骨增厚更加明显,空泡细胞层达7～12层,骨小梁周围有显著增生的成骨细胞。证实低钙时股骨干骺端生长板软骨有明显组织形态改变。低钙使长骨生长板软骨细胞肥大层增生增厚、成骨细胞增生,是否低钙使终末软骨细胞死亡减少,以及如何使成骨细胞生长调节异常尚待研究。     

锌缺乏对大鼠骨骼矿化的影响

目的　探讨缺锌对大鼠骨骼矿化的影响。方法　将 30只Wistar大鼠按体重随机分为缺锌组、对照组和对喂组 ,每组 10只。缺锌组饲料锌含量为 3 9mg/kg ,对照组饲料锌含量为 2 4 7mg/kg,对喂组饲对照组饲料 ,饲料摄入量与缺锌组相同。运用骨组织形态计量学方法测量骨骼矿化相关指标、测定股骨矿物质含量、骨密度、骨中锌、钙、磷、镁、锰、铜元素和骨骼羟脯氨酸含量及血中甲状旁腺激素、降钙素和骨钙素含量。结果　缺锌组大鼠与对照组和对喂组相比 ,骨矿化沉积速率、股骨磷、锌、骨羟脯氨酸及血清降钙素、骨钙素含量显著降低 ,缺锌组相应指标分别为 :( 3 2 6± 0 34) μm/d、( 6 4 5 4± 2 34)g/kg、( 5 4 4± 9 5 )mg/kg、( 9 2 8± 1 6 2 )g/kg、( 41 2± 13 5 ) μg/L、( 82± 30 ) μg/L ;对照组分别为 :( 5 37± 0 5 3) μm/d、( 6 9 0 1± 4 0 5 )g/kg、( 117 4± 8 0 )mg/kg、( 11 31± 1 30 )g/kg、( 6 8 3± 14 4)μg/L、( 131± 46 ) μg/L ;对喂组分别为 :( 5 45± 0 30 ) μm/d、( 6 7 81± 3 5 6 )g/kg、( 10 6 7± 8 4)mg/kg、( 10 88± 1 47)g/kg、( 6 3 7± 12 0 ) μg/L、( 12 0± 5 2 ) μg/L。骨矿化延迟时间和骨基质成熟时间显著增加 ,缺锌组相应指标分别为 :( 1 0 8± 0 19)     

亚慢性氟染毒对大鼠骨组织病理改变和β-连环蛋白表达的影响

目的观察亚慢性氟染毒对大鼠骨组织中β-连环蛋白表达的影响,探讨β-连环蛋白在氟致骨损伤中的可能作用。方法 40只Wistar大鼠按体重随机分成4组,染氟组大鼠饮用含氟50、100和150mg/L的自来水,对照组大鼠饮用自来水,3个月后测定大鼠血清及骨组织氟含量,Real-time RT-PCR法和免疫组化法检测骨组织中β-连环蛋白mRNA和蛋白质表达情况。结果 HE染色显示染氟组大鼠病理学改变呈现骨皮质增厚、骨小梁增多等骨硬化表现,骺板肥大软骨细胞大量堆积且排列紊乱。染氟组大鼠骨组织中β-连环蛋白mRNA表达显著高于对照组,差异有统计学意义(P<0.01),而且随染毒剂量升高,β-连环蛋白mRNA表达逐渐升高。免疫组化显示染氟组大鼠骨组织中β-连环蛋白主要由成骨细胞和破骨细胞表达,骺板软骨肥大细胞也有阳性表达。结论β-连环蛋白在亚慢性氟染毒大鼠骨质硬化的发生中发挥重要作用。     

魔芋精粉对大鼠钙磷代谢和骨骼的影响

本文用含１％魔芋精粉的饲料喂饲大鼠１８个月，观察魔芋精粉对钙磷代谢和骨骼的影响。结果表明，食用魔芋精粉组与对照组的血清钙磷含量、股骨重和骨钙磷含量以及骨形态计量参数（骨小梁体积、骨小梁周长、类骨质周长、类骨质表面、骨皮质厚度），两组间均无显著性差异。以上结果说明大鼠长期摄入含１％的魔芋精粉饲料，对钙磷代谢及骨骼未见不良影响。     

维生素K_2和染料木黄酮对去势大鼠骨代谢的作用比较

目的维生素K2和染料木黄酮对去势大鼠的骨代谢作用比较。方法将雌性Wistar大鼠40只随机分为5组:假手术组,去势对照组、去势+雌激素组(己烯雌酚,20μg/kg.d)、去势+维生素K2(25 mg/kg.d)组、去势+染料木黄酮(25 mg/kg.d)组,每组8只。饲养3个月后处死,进行骨密度、骨组织形态学参数、血清骨钙素和尿脱氧吡啶啉含量的测定。结果与假手术组相比,去势组大鼠股骨骨密度显著降低、骨小梁体积和密度减少、骨小梁间隙增大,血清骨钙素和尿脱氧吡啶啉含量明显增高;与去势组相比,维生素K2和染料木黄酮组骨小梁体积和密度增加,股骨骨密度无显著变化;维生素K2组骨小梁间隙减少,而染料木黄酮组无显著变化;维生素K2和染料木黄酮组尿脱氧吡啶啉含量明显降低。结论维生素K2和染料木黄酮通过抑制骨吸收,减少去势大鼠骨小梁骨量丢失,预防骨质疏松的发生。但维生素K2可减少骨小梁间隙,而染料木黄酮无此作用。因此,维生素K2预防骨质疏松作用强于染料木黄酮。     

锌缺乏对孕鼠发育及体内促生长有关激素水平的影响

目的　探讨锌缺乏对妊娠大鼠发育及体内促生长有关激素含量的影响。方法　将Wistar妊娠大鼠随机分为缺锌组 (ZD)、对喂组 (PF)、补锌组 (ZS)及正常对照组 (Cont) ,分别给予缺锌 (0 .7mg/ kg)和正常锌 (1 0 0 mg/ kg)饲料喂养 ,观察孕鼠及胎鼠发育情况 ,并采用放射免疫法检测血清中甲状腺素 (T3 、T4 )、促甲状腺素 (TSH)和生长激素 (GH)含量。结果　缺锌组孕鼠在妊娠期间体重没有增加 ;胎鼠出生体重显著低于其他三组 ;血清中激素含量显著低于补锌组和正常对照组。结论　锌缺乏可降低孕鼠血液中促生长有关激素含量 ,导致孕鼠及胎儿生长发育迟缓。     

缺锌并补锌对大鼠睾丸及血清睾酮的影响

目的　为了解锌缺乏及补锌对大鼠睾丸的重量及血清睾酮的影响。　方法　将出生后断乳一周的SD大鼠随机分为缺锌组、配喂组、对照组、补锌组和高锌组五组 ,缺锌组、对照组和高锌组分别用缺锌饲料 (锌含量 <1mg/kg)、常锌饲料 (锌含量为 5 0mg/kg)和高锌饲料 (锌含量为 15 0mg/kg)喂养 8周 ,补锌组用缺锌饲料喂养三周后改用高锌饲料喂养五周 ,配喂组用常锌饲料喂养 ,给料量按缺锌组前一天实际进食量添加。 8周后处死 ,用极谱法测定血清中锌含量 ,用原子吸收分光光度法测定睾丸中锌含量 ,采用双抗体放射免疫分析法测定血清中睾酮的含量。　结果　缺锌组大鼠睾丸及血清中锌含量降低 ,睾丸重量减轻。血清中睾酮含量下降 ,缺锌大鼠补锌后可恢复正常。　结论　说明锌缺乏直接影响睾丸及血清中锌的水平 ,从而影响大鼠睾丸的发育及睾酮的分泌与合成。     

Fermented soybean product (Cheonggukjang) improved some attributes of protein and growth hormone measurements in Sprague-Dawley rats

We hypothesized that the administration of Cheonggukjang (CKJ) would exert positive effects on factors implicated with growth in Sprague-Dawley (SD) rats. To test this hypothesis, we measured specific aspects of bone and organ growth in male SD rats that were treated for 6 weeks with 3 concentrations of CKJ. Although the CKJ extract contained high concentrations of flavonoids and phenolic compounds, no significant differences in body length, organ weights, or femur weight were detected between the CKJ- and vehicle-treated groups. However, thicknesses of the epiphyseal growth plate in the proximal femoral epiphysis and the compact bone in the linea aspera were broadest in the femur of the 2 CKJ-treated groups when compared with the vehicle-treated groups. Furthermore, the levels of growth hormone (GH) and calcium ion were higher in the sera of the high-concentration CKJ–treated groups, whereas the expression level of GH receptor was higher in muscle tissue of all CKJ-treated groups and in the liver tissue of the high-concentration CKJ–treated group. In the GH receptor downstream signaling pathway, the phosphorylation levels of Akt and Erk were expressed differently between liver and muscle tissues upon CKJ treatment. However, the phosphorylation level of STAT5 was very similar to the expression level of the GH receptor in all CKJ-treated groups. These results indicate that CKJ extract may increase the thickness of the epiphyseal growth plate and the compact bone of the femur, elevate GH secretion, and stimulate regulation of the GH receptor downstream signaling pathway in the liver and muscle tissues of SD rats.     

Reduced growth and skeletal changes in zinc-deficient growing rats are due to impaired growth plate activity and inanition

We investigated the effects of dietary zinc deficiency on skeletal metabolism in an animal model. Thirty 21-d-old male Sprague-Dawley rats were fed for 28 d either a zinc-deficient (ZD) diet (1 mg zinc/kg) or a normal diet ad libitum (AL, 50 mg zinc/kg) or in the same quantity as the ZD (pair-fed, PF). Only in the ZD group were general physical signs of zinc deficiency observed. Compared with the AL and PF rats, ZD rats showed significantly lower mean values in ponderal growth rate, femur weight and length, circulating levels of insulin-like growth factor-I, bone mechanical properties and concentration of zinc and, on histomorphometry, a decrease in the thicknesses of the overall growth plate and hypertrophic cartilage. In contrast, although bone volume was significantly lower in the ZD and PF rats than in the AL rats, no difference was observed between the ZD and PF rats. Osteoclast surface/bone surface and osteoclast number/bone surface ratios were significantly greater in PF rats than in the other two groups and not different in ZD and AL rats. Collectively, these data indicate that zinc deficiency has profound effects on the skeletal system of growing rats. In particular, the effects of zinc deficiency on bone growth and mass are the result of the reduced activity of the growth plate, likely mediated by impairment in the insulin-like growth factor-I system. We did not demonstrate an effect on bone mass via increased bone resorption.     

Effect of thyroxine injection on bone growth in malnourished rats at different growth stages

This study investigated the role of thyroxine on bone growth by injecting it into malnourished weaned and suckling rats. Weaned rats were fed a normal diet or a low-protein, low-energy diet, and injected with saline or thyroxine (5 micrograms/100 g BW) for 22 days. Suckling pups were injected with saline or 2 micrograms of thyroxine, and reared by dams fed a normal diet or a low-protein diet for 15 days. Thyroxine injection decreased body weight gain in both growth stages. Bone length, width and weight were not affected by thyroxine injection in weaned rats. Thyroxine injection increased femur length and tail growth, but did not change bone width in suckling rats. The epiphyseal growth plate and zone of hypertrophic cartilage cells were thinner in malnourished rats than in normal rats at both growth stages, but the number of proliferating chondrocytes was greater in suckling rats that received thyroxine injections than in those that received saline injections. The disappearance of trabeculae was observed in both normal and malnourished weaned rats upon thyroxine injection. These results suggested that retarded bone growth due to malnutrition might be independent of thyroid function in both growth stages.     

The influence of protein and/or energy deficiency on the growth of long bone in rats

The effects of protein and/or energy deficiency on long bone growth were studied using rats of an average weight 100g. Four groups of Wistar rats were respectively fed on a normal diet, a low-energy diet, a low protein-diet, and a low-protein and low-energy diet for 45 days. Both energy and protein deficiency restricted gains of body weight and femur length and the activity of alkaline phosphatase in the tibia to the same extent. The epiphyseal growth plates of the femur in protein-deficient rats were as thin as those in energy-deficient rats. On the other hand, femur width and activity of acid phosphatase in the tibia were lower in protein-deficient animals than those in energy-deficient ones. Serum calcium concentrations and calcium content of bone were the same among all groups.     

Short-term zinc deficiency inhibits chondrocyte proliferation and induces cell apoptosis in the epiphyseal growth plate of young chickens

The purpose of this study was to investigate the effect of zinc deficiency on chondrocyte proliferation, differentiation and apoptosis in the epiphyseal growth plate of juvenile chickens. Newly hatched broiler chickens were fed either a low zinc (10 mg/kg diet) or a zinc-adequate (68 mg/kg diet) soy protein-based purified diet. Cell proliferation in the growth plate was evaluated with bromodeoxyuridine (BrdU) labeling. Apoptosis was assessed using the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) method. Chondrocyte differentiation was evaluated with immunostaining of osteonectin as a marker of maturation. As early as d 3 of feeding, zinc deficiency significantly inhibited chondrocyte proliferation, promoted cell differentiation and induced cell apoptosis in the growth plate. These effects were manifested primarily in areas remote from the blood supply. Immunostaining for local growth factors such as insulin-like growth factor-1 (IGF-1), parathyroid hormone-related protein (PTHrP) and fibroblast growth factor-2 (FGF-2) did not reveal any differences between growth plates of zinc-deficient and zinc-adequate chickens after 3 d of feeding. By d 7, severe growth plate lesions characterized by reduced cellularity and abnormally shaped cells were formed in areas remote from blood vessels. Immunoreactive IGF-1, PTHrP and FGF-2 were all greatly reduced in the lesion. However, the growth rate and food intake of zinc-deficient chickens were not different from those of the controls during the 7-d experiment. Therefore, a direct effect of zinc deficiency on proliferation, differentiation, and apoptosis of growth plate chondrocytes was indicated.     

大豆异黄酮类对去卵巢大鼠骨丢失的影响

目的　研究大豆中植物雌激素——异黄酮类对去卵巢大鼠骨丢失的预防作用。方法　将 3月龄 SD雌性大鼠按体重分为 5组 ,每组 1 1只 :假手术对照组 (假手术 +饲含酪蛋白饲料 ,Sham) ;去异黄酮组 (去卵巢 +饲含去异黄酮类大豆分离蛋白饲料 ,Soy- ) ;异黄酮组 (去卵巢 +饲含异黄酮类大豆分离蛋白饲料 ,Soy+) ;酪蛋白组 (去卵巢 +饲含酪蛋白饲料 ,即去卵巢对照组 ,Ovx) ;雌激素对照组 (去卵巢 +饲含酪蛋白饲料 +注射雌二醇 ,E2 )。在实验期第 3周、第 6期和第 9周各进行为期三天的钙代谢试验。第 1 0周末处死大鼠 ,测定骨钙、骨密度 ,并对股骨远端松质骨进行骨组织形态学测量。结果　异黄酮组和雌激素对照组粪钙、尿钙排出量显著低于酪蛋白组和去异黄酮组 (P<0 .0 5) ,钙表观吸收率和钙贮留量显著高于酪蛋白组和去黄酮组 (P<0 .0 5) ,钙代谢呈正平衡。异黄酮组和雌激素对照组骨钙、骨密度高于酪蛋白组和去异黄酮组 (P<0 .0 5)。与雌激素对照组比较 ,异黄酮组骨小梁面积百分率和骨小梁数目明显减少 ,骨小梁间隙明显增宽 (P<0 .0 5) ;但与酪蛋白组和去异黄酮组比较 ,异黄酮组骨小梁面积百分率和骨小梁数目明显增多 ,骨小梁间隙明显减少 (P<0 .0 5)。结论　含有异黄酮类的大豆分离蛋白具有预防骨丢失的作用 ,而?