青年去势及老龄雌性大鼠骨质疏松模型比较及其临床护理意义

目的建立青年去势及老龄雌性大鼠骨质疏松模型，探讨两种雌性大鼠骨质疏松模型骨组织微观结构、骨矿及骨负荷改变情况及潜在机制．为女性骨质疏松的临床护理干预寻找相应的理论依据。方法32只1月龄雌性Sprague Dawley（SD）大鼠。同等条件下饲养，饲养至4个月按体重随机分成青年去势及假手术对照组大鼠16只、老龄雌性及对照组大鼠16只，进行去势及老龄骨质疏松造模。比较青年去势组（Ovariectomized rats．8只，OVX组）和老龄骨质疏松组（Senile Female Osteoporotic Rats．8只．SF组）大鼠骨质改变情况。结果OVX组大鼠去卵巢8周出现骨质疏松改变，SF组大鼠22月龄自然衰老出现骨质疏松改变。OVX组骨小梁宽度显著大于SF组（P〈0．05）；两组模型之间腰椎及股骨密度差异不显著（均P〉0．05），但OVX组股骨最大负荷显著高于SF组（P〈0．01）；OVX组骨钙水平显著高于SF组（P〈0.01）．但两组血钙水平差异不显著（P〉0．05）。结论4月龄大鼠去卵巢8周以及自然饲养22月龄雌性大鼠可分别作为女性绝经后及老年女性骨质疏松的模型。老龄骨质疏松模型在骨微观结构、骨生物力学特性、骨矿水平含量方面的负性改变更甚于青年去势模型。提示对女性骨质疏松症患者的护理干预措施应侧重于不同年龄阶段及骨代谢特点进行。     

小麦喷硒对大骨节病儿童指骨干骺端与骨端X线病变修复作用的研究

本文报道了补硒对大骨节病儿童指骨干骺端与骨端X线病变修复作用的5年试验研究,结果为补硒对大骨节病干骺端病变有一定促进修复的作用,对于骨端病变,硒的修复作用不明显,干骺端病变用硒治愈或愈后仍可发生骨端的病变。由于目前大骨节病有自然下降及硒含量自然上升的趋势,作者认为决策补硒时,应在人群体内硒水平低且大骨节病仍有新发的病区中进行。     

老龄骨质疏松骨形态、骨密度、生物力学实验研究

[目的]观察自然衰老骨质疏松模型中雌性大鼠骨形态、骨密度、骨生物力学改变,探索老年妇女骨质疏松症发生发展的机制.[方法]选择健康纯种雌性SD大鼠10只,喂养22月后复制自然衰老骨质疏松模型,另随机选择6月龄雌性大鼠10只为青年对照组,观察其骨形态、骨密度、骨生物力学指标.[结果]与青年对照组比,骨质疏松组骨小梁面积百分比显著降低(50%,P＜0.05),股骨平均骨小梁数显著减少(65%,P＜0.05),平均骨小梁宽度显著变窄(27%,P＜0.05).②骨质疏松组股骨与椎骨骨密度(64.3±8.1 g/cm2,59.3±15.1 g/cm2)较青年对照组(81.8±7.2 g/cm2,92.2±6.1g/cm2)显著降低(P＜0.05),椎骨骨密度下降得更明显(35.7%比21.3%).③骨质疏松组股骨与椎骨的最大负荷力(134.41±23.52N,235.0±12.2N)较青年对照组(155.81±17.84N,327.1±24.8N)显著降低(P＜0.05),且椎骨的最大负荷力降低更明显(28%比14%).骨质疏松组椎骨、股骨的最大应变(1.28±0.12 mm,1.6±0.15 mm)与青年对照(1.38±0.15mm,1.81±0.21 mm)比有明显下降的趋势,但尚未形成统计学差异.[结论]老年雌性大鼠骨质疏松症中骨形态发生、骨密度明显改变,骨形态学、变化更能反映早期的骨结构的变化,这种变化发展下去可能会影响骨的力学性能.     

增龄性变化对大鼠骨质量、血清骨代谢指标影响研究

[目的]探讨增龄性变化对大鼠骨质量、血清骨代谢指标的影响。[方法]14只新生雄性Sprague Dawley（SD）大鼠，同等条件下饲养，饲养至6个月按体重随机分为老龄骨质疏松组（AO组）和青年对照组（YC组），将YC组安乐处死，AO组继续饲养至22个月，两组大鼠均取左侧股骨，测量骨密度、骨组织形态计量学指标，以及骨矿水平及骨代谢指标。[结果]腰椎及股骨密度（BMD）在老龄大鼠均下降，其中股骨密度下降尤其显著（P〈0.01）。与YC组比较，AO组大鼠骨钙素水平显著降低（P〈0.01），抗酒石酸酸性磷酸酶（TRACP）水平显著升高（P〈0.05）；骨生物力学测定发现，AO组大鼠的股骨最大受力负荷下降。骨形态计量学测定发现，AO组大鼠骨小梁体积、骨小梁宽度、骨皮质厚度显著下降（P〈0.05或P〈0.01），骨小梁间隙增大（P〈0.01），AO组大鼠骨小梁普遍变薄、变细甚至断裂穿孔。[结论]22月龄雄性大鼠发生了骨质疏松的变化，骨形成降低，骨矿含量下降，骨微观组织结构破坏。     

"中药硼复方"对摄入过量氟实验大鼠骺板软骨损伤的预防作用

为观察和分析中药硼复方对摄入过量氟实验大鼠骺板软骨损伤的预防作用,将SD大鼠随机分为对照组,过量氟组,中药硼复方预防组,实验后10w测定血清游离氟和骨氟含量,血清硼含量,胫骨纵径横径和重量,肋骨和肋软骨RNA含量,观察胫骨骺板软骨的组织形态学变化,结果显示与对照组比较,过量氟组大鼠血清游离氟和骨氟含量增加,胫骨纵径,横径减轻,干重减轻,肋骨和肋软骨总RNA含量减低,胫骨骺板软骨出现明显病理变化,预防组大鼠较过量氟组大鼠血清游离氟和骨氟含量降低,胫骨纵径,横径和干重及肋骨和肋软骨总RNA含量明显增加,胫骨骺板软骨损害减轻,说明中药硼复方对过量氟实验大鼠骺板软骨损伤有一定的预防作用。     

过量氟对实验大鼠软骨细胞分化及Ⅱ和Ⅹ型胶原表型表达的影响

目的观察过量氟对实验大鼠骺板软骨和关节软骨Ⅱ和Ⅹ型胶原表型表达及细胞分化的影响,探讨过量氟对软骨发育的影响和氟骨症的发病机制.方法 60只SD大鼠,随机分为对照组(19只,饮蒸馏水)、低过量氟组(20只,饮水氟浓度为50 mg/L),高过量氟组(21只,饮水氟浓度为100 mg/L).实验10周和20 周时,处死大鼠取胫骨关节软骨和骺板软骨,HE染色,Ⅱ、Ⅹ型胶原单克隆抗体免疫组织化学法测定软骨Ⅱ、Ⅹ型胶原表型表达变化.结果随饮水中过量氟浓度的增高,大鼠胫骨骺板软骨增生层、肥大层细胞滞留,关节软骨出现散在软骨细胞坏死;过量氟大鼠软骨Ⅱ型胶原在骺板软骨滞留或增生过度的增生层和肥大层中表达,在关节软骨中表达减少;Ⅹ型胶原在滞留的肥大软骨细胞区,突入先期钙化带中的软骨半岛、软骨岛和骨化岛边缘表达;高过量氟组大鼠关节软骨表、中层Ⅹ型胶原表达增强.结论过量氟对大鼠软骨细胞分化有两种结果:四肢骺板软骨增生层、肥大层软骨细胞分化过度而滞留,加之基质矿化障碍,导致骨软化发生;高过量氟组大鼠关节软骨Ⅱ型胶原表型表达减少,Ⅹ型胶原表型表达增强,趋向骨关节病发生.     

镓盐对维甲酸致大鼠骨质疏松模型影响的实验研究

目的 研究镓盐对维甲酸致骨质疏松大鼠骨代谢的影响,为镓盐治疗骨质疏松提供实验依据。方法 用维甲酸建立大鼠骨质疏松模型,并通过氯化镓灌胃给药治疗两个月,应用生化、病理等方法研究其对反映骨质疏松相关指标的影响。结果 维甲酸可导致大鼠骨结构改变,密度降低,骨有基质含量下降,血清抗酒石酸酸性磷酸酶（TPAP）上升。应用氯化镓后,可增加骨密度,增加骨皮质厚度和骨小梁百分比,降低TRAP活性和碱性磷酸酶（AKP）活性,从而降低骨转换率。结论 镓盐是一种有效的降低骨转换率的药物。     

低硒、低碘及联合对亲代和子代大鼠骨、软骨生长的影响

Objective To study the effects of selenium deficiency,iodine deficiency and combined selenium and iodine deficiency on bone and cartilage growth in the parental and the first filial generation rats. Methods Forty-eight weanling healthy SD rats were randomly divided into selenium deficieney, iodine deficiency, combined selenium and iodine deficiency and control groups according to their body mass. These rats were fed with selenium deficiency, iodine deficiency, combined selenium and iodine deficiency, and normal fodder, respectively. The parental rats (about 3 months old) were mated in each group 8 weeks after the beginning of the experiment. Right tibias and left knee joints were collected when the parental generation rats were about 6 months and the first filial generation rats were about 3 months old. Tibial length, mid-shaft tibial diameter, and articular cartilage diameters of the right tibias were measured by vernier caliper. Left knee joints were embedded and cut into sections and the thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes in growth plate cartilage were observed under the light microscope. Results The selenium deficiency had significant effect on serum selenium level of the parental and the first filial generation rats(F value were 239.56,232.68, P< 0.01), and also on serum T4 level of the first filial generation rats(F value were 6.95, P < 0.05). The iodine deficiency had significant effect on serum T3 and T4 level in the two generations rats(F value were 14.11,14.05,30.29,34.53, P < 0.01 ). There were interactions between selenium deficiency and iodine deficiency on serum T4 level in the first filial generation rats (F= 5.99, P< 0.05). The serum selenium of selenium deficiency group[ (30.28 ± 6.34), (43.95 ± 9.75)μg/L],combined selenium and iodine deficiency group[ (30.33 ± 5.18), (35.40 ± 3.16)μg/L] were significantly lower than iodine deficiency group[(345.83 ± 29.55), (245.24 ± 9.95)μg/L] and the controls[ (358.64 ± 30.50), (236.50 ±9.75) μg/L] in the two generations. The serum T3 of combined selenium and iodine deficiency group [(0.55 ± 0.05 ),(0.88 ± 0.14)nmol/L] were significantly lower than the controls[(0.75 ± 0.08), (1.26 ± 0.26)nmol/L] in the two generations. The serum T4 of iodine deficiency [ (24.11 ± 2.29), (42.10 ± 8.92) nmol/L ] and combined selenium and iodine deficiency group[ (20.66 ± 1.93), (26.55 ± 5.98)nmol/L] were significantly lower than the controls[ (36.15 ±2.74), (52.79 ± 8.84)nmol/L] and selenium deficiency group[ (28.12 ± 3.33), (52.02 ± ll.99)nmol/L] in the two generations. The selenium deficiency and iodine deficiency had significant effect on tibial length, thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes in first filial generation rats(F values were 24.31,6.98,40.76,56.15,25.24,82.82, 10.07,5.57, P <0.05 or <0.01). There were interactions between selenium deficiency and iodine deficiency on tibial length, thickness of the growth plate cartilage, layers of proliferative and hypertrophic chondrocytes (F values were 5.68,24.86,41.82,9.12, P <0.05 or <0.01 ). The tibial length of the selenium deficiency group[ (33.17 ± 0.34)mm] and combined selenium and iodine deficiency group[ (31.30 ± 0.87)mm] were significantly lower than the controls[ (34.12 ± 0.32)mm, P< 0.05]. Thickness of the growth plate cartilage [ (1.60 ± 0.18)mm ], layers of proliferative chondrocyte (8.54 ± 0.81), and hypertrophic chondrocyte (4.95 ± 0.37)of the combined selenium and iodine deficiency group were significantly decreased when compared to the selenium deficiency group[ (3.03 ± 0.10)mm, 14.68 ± 0.84,6.60 ± 0.31], iodine deficiency group[ (2.90 ± 0.09)mm, 13.75 ±0.33,6.61 ± 0.84 ] and the controls [ (3.19 ± 0.09) mm, 14.94 ± 0.36, 6.64 ± 0.26, P <0.05]. Thickness of the growth plate cartilage, layers of proliferative chondrocyte of the iodine deficiency group were lower than the controls(P<0.05). Conclusions Selenium deficiency impair tibial growth in first filial generation rats, iodine deficiency retarded the chondroncyte proliferation and decreases the thickness of growth plate cartilage in first filial generation rats, and combined selenium and iodine deficiency significantly impair the growth of bone and cartilage in first filial generation rats.     

过量氟对大鼠部分组织中钙、镁、磷水平的影响

目的：研究慢性氟中毒大鼠在不同染氟剂量及时间内，体内不同组织中钙（Ca)、镁（Mg)、磷（P）水平的变化，探讨过量氟对不同组织中各元素水平的影响。方法：SD大鼠70只分为对照组和低，中，高剂量染氟组，观察实验后3个月（42只）和5个月（28只）的变化。低钙喂养，3个月及5个月后，取氟中毒大鼠心、肝、肾、脾、肌肉、四肢骨及血清，分析，分析F,Ca,P,Mg含量，结果：大鼠氟后各组织氟含量均有不同程度升高，随时间不同，组织中的氟含量呈现动态过程，经多元逐回归分析，大鼠染氟3个月后肌肉中F与Ca,P，肝脏中F与Mg，四肢骨中F与Mg，心脏中F与Ca呈显著性相关（P＜0．05），染氟5个月后肝脏中F与Ca，四肢骨中F与Mg，心脏中F与Ca，肾脏中F与P，Mg呈显著性相关（P＜0．05）。结论：氟中毒大鼠不同组织中相关元素含量随染氟剂量，时间不同而不同。     

钙剂及甲基睾丸酮对老龄雄性大鼠股骨计量形态学及骨矿的影响

目的 探讨钙剂、甲基睾丸酮对老龄雄性大鼠骨质疏松的作用效果及其发生机制,为老年男性骨质疏松的临床干预寻找理论依据.方法 26只新生雄性Sprague Dawley(SD)大鼠,按体重随机分成老龄对照组、青年对照组、葡萄糖钙组(2.5 mg/kg·d)及甲基睾丸酮组(25 mg/kg·d),同等条件下饲养,青年对照组饲养至6个月,其余3组饲养至22个月后,对其中两组开始分别连续给药92 d.经处理后,取左侧股骨,用双光子骨密度仪测定骨密度;北航半自动彩色图像分析系统进行骨组织形态计量学分析,测量骨小梁体积、骨小梁宽度、骨小梁间隔、骨皮质厚度;原子吸收分光光度法及钼兰比色法检测各组大鼠骨钙、骨磷的浓度.结果 22月龄雄性大鼠可作为自然衰老骨质疏松的实验模型;与老龄对照组比较,葡萄糖酸钙组和甲基睾丸酮组大鼠股骨密度、骨小梁体积、骨小梁宽度及皮质厚度增加(P<0.05),骨小梁间隙缩小(P<0.05),骨矿化水平提高(P<0.05).结论 补充钙剂和甲基睾丸酮可增加股骨密度及骨矿化水平,促进老龄雄性大鼠股骨形态学的改善.