中国组织工程研究
中國組織工程研究
중국조직공정연구
Journal of Clinical Rehabilitative Tissue Engineering Research
2013年
28期
5113-5119
,共7页
鲍小明%王云%侯永新%李军%张民%卫小春
鮑小明%王雲%侯永新%李軍%張民%衛小春
포소명%왕운%후영신%리군%장민%위소춘
组织构建%骨组织构建%去势大鼠%骨质疏松%血管内皮生长因子%成骨细胞%骨密度%股骨干骺端%省级基金
組織構建%骨組織構建%去勢大鼠%骨質疏鬆%血管內皮生長因子%成骨細胞%骨密度%股骨榦骺耑%省級基金
조직구건%골조직구건%거세대서%골질소송%혈관내피생장인자%성골세포%골밀도%고골간후단%성급기금
tissue construction%bone tissue construction%ovariectomized rat%osteoporosis%vascular endothelial growth factor%osteoblasts%bone mineral density%femoral metaphysic%provincial grants-supported paper
背景:血管内皮生长因子在促进骨质疏松性骨折愈合中发挥重要作用,而它是否影响骨密度变化还没明确。目的:观察去势大鼠血清血管内皮生长因子水平和骨密度及成骨细胞变化的相关性。方法:SD 雌性大鼠40只随机数字表法均分为去势组和对照组,3个月后测大鼠全身、腰椎及股骨骨密度。大鼠 ELISA 试剂盒测血清中血管内皮生长因子的水平,同时两组大鼠股骨干骺端固定,脱钙,脱水、石蜡包埋、切片,苏木精-伊红染色,每切张片随意取5个视野(10×40)行股骨远侧干骺端成骨细胞计数在光学显微镜。结果与结论:去势3个月后大鼠体质量明显增加(P <0.05),去势组全身、腰椎及股骨骨密度较对照组全身、腰椎及股骨骨密度降低(P <0.05),表明骨质疏松的模型建立。而去势大鼠和对照大鼠血管内皮生长因子水平比较差异无显著性意义(P >0.05),去势组及对照组的成骨细胞数量无明显差异(P >0.05),去势组及对照组骨密度与成骨细胞数及血清血管内皮生子水平无相关性。提示去势大鼠的骨密度下降,体质量升高,而去势大鼠骨密度的降低与血清血管内皮生长因子变化可能无关。
揹景:血管內皮生長因子在促進骨質疏鬆性骨摺愈閤中髮揮重要作用,而它是否影響骨密度變化還沒明確。目的:觀察去勢大鼠血清血管內皮生長因子水平和骨密度及成骨細胞變化的相關性。方法:SD 雌性大鼠40隻隨機數字錶法均分為去勢組和對照組,3箇月後測大鼠全身、腰椎及股骨骨密度。大鼠 ELISA 試劑盒測血清中血管內皮生長因子的水平,同時兩組大鼠股骨榦骺耑固定,脫鈣,脫水、石蠟包埋、切片,囌木精-伊紅染色,每切張片隨意取5箇視野(10×40)行股骨遠側榦骺耑成骨細胞計數在光學顯微鏡。結果與結論:去勢3箇月後大鼠體質量明顯增加(P <0.05),去勢組全身、腰椎及股骨骨密度較對照組全身、腰椎及股骨骨密度降低(P <0.05),錶明骨質疏鬆的模型建立。而去勢大鼠和對照大鼠血管內皮生長因子水平比較差異無顯著性意義(P >0.05),去勢組及對照組的成骨細胞數量無明顯差異(P >0.05),去勢組及對照組骨密度與成骨細胞數及血清血管內皮生子水平無相關性。提示去勢大鼠的骨密度下降,體質量升高,而去勢大鼠骨密度的降低與血清血管內皮生長因子變化可能無關。
배경:혈관내피생장인자재촉진골질소송성골절유합중발휘중요작용,이타시부영향골밀도변화환몰명학。목적:관찰거세대서혈청혈관내피생장인자수평화골밀도급성골세포변화적상관성。방법:SD 자성대서40지수궤수자표법균분위거세조화대조조,3개월후측대서전신、요추급고골골밀도。대서 ELISA 시제합측혈청중혈관내피생장인자적수평,동시량조대서고골간후단고정,탈개,탈수、석사포매、절편,소목정-이홍염색,매절장편수의취5개시야(10×40)행고골원측간후단성골세포계수재광학현미경。결과여결론:거세3개월후대서체질량명현증가(P <0.05),거세조전신、요추급고골골밀도교대조조전신、요추급고골골밀도강저(P <0.05),표명골질소송적모형건립。이거세대서화대조대서혈관내피생장인자수평비교차이무현저성의의(P >0.05),거세조급대조조적성골세포수량무명현차이(P >0.05),거세조급대조조골밀도여성골세포수급혈청혈관내피생자수평무상관성。제시거세대서적골밀도하강,체질량승고,이거세대서골밀도적강저여혈청혈관내피생장인자변화가능무관。
BACKGROUND: Vascular endothelial growth factor play an important role in promoting healing of osteoporotic fractures, but whether it can affect the bone mineral density is not clear. OBJECTIVE: To observe the correlation between serum vascular endothelial growth factor, bone mineral density and the number of osteoblasts in the ovariectomized rats. METHODS: Forty female Sprague-Dawley rats were randomly divided into ovariectomized group and control group. After 3 months, the bone mineral density of the whole body, femur and lumbar spine was measured. Rat enzyme-linked immunosorbent assay kit was used to measure the level of serum vascular endothelial growth factor. Then, the rats in two groups received femoral metaphyseal fixation, decalcified, dehydrated, embeding in paraffin, slicing and hematoxylin-eosin staining. Each slice was free to take five fields of view (10×40) in order to count the osteoblasts of femur distal metaphysis under optical microscope. RESULTS AND CONCLUSION: After ovariectomized for 3 months, the rats body mass was increased significantly (P < 0.05), and the bone mineral density of the whole body, femur and lumbar spine in the ovariectomized group was lower than that in the control group (P < 0.05), indicating the successful establishment of osteoporosis model. There was no significant difference in vascular endothelial growth factor level between the ovariectomized group and the control group (P > 0.05), and the difference of the osteoblast number between ovariectomized group and control group was not significant (P > 0.05). This indicated that there was no correlation between bone mineral density and the number of osteoblasts and vascular endothelial growth factor level in the ovariectomized group and the control group. These findings suggest that the bone mineral density is reduced and the body mass is increased in the ovariectomized rats, and the reduced bone mineral density of ovariectomized rats may be irrelevant with the change of serum vascular endothelial growth factor.