CAJ | 학술논문

背景:研究表明承载丸治疗激素性股骨头坏死具有明确的疗效.可明显增加骨密度、骨重量、骨强度和刚性,能改变雌激素水平低下状态.目的:观察承载丸对激素性股骨头坏死大鼠骨细胞中细胞黏附分子基因的影响,以明确该药对坏死股骨头内血管恢复正常血运的作用.设计、时间及地点:分组对照观察,于2006-03/08在中国中医科学院望京医院药理实验室及生物芯片北京国家工程研究中心所属博奥芯片公司实验室完成.材料:6月龄雄性SD大鼠6只,体质量(280±20)g.承载丸主要成分:有当归,杜仲,黄芪,枸杞子,鹿角霜,肉苁蓉、地鳖虫,水蛭、丹参,续断等22味中药.由北京市勃然制药有限公司提供.方法:6只SD大鼠采用内毒素和甲基强地松龙制做激素性股骨头坏死动物模型,随机将大鼠分为模型组和承载组,每组各3只.承载组大鼠自第1次注射甲基强地松龙后,灌服承载丸药液1.5g/kg,1次/d,共灌服6周.6周后取股骨头提取总RNA,进行基因谱测试.主要观察指标:基因谱测试结果中的细胞黏附分子基因作用路径分析.结果:3只模型大鼠使用承载丸后,与模型大鼠相比较,出现1.5倍以上改变的基因,分别为633个(下调506个,上调127个)、883个(下调640个,上调243个)、593个(下调408个,上调185个).使用MAS软件归类分析后,共有相关作用路径79个,涉及297个基因.其中细胞黏附分子路径有8个下调基因.结论:大鼠服用承载丸后,使上述基因下调,恢复了大鼠巨噬细胞及靶细胞的识别功能,恢复了上皮细胞包括血管内皮细胞的正常生存条件,细胞黏附分子作用路径持正常水平,这是坏死股骨头内血管恢复正常血运的关键.
배경:연구표명승재환치료격소성고골두배사구유명학적료효.가명현증가골밀도、골중량、골강도화강성,능개변자격소수평저하상태.목적:관찰승재환대격소성고골두배사대서골세포중세포점부분자기인적영향,이명학해약대배사고골두내혈관회복정상혈운적작용.설계、시간급지점:분조대조관찰,우2006-03/08재중국중의과학원망경의원약리실험실급생물심편북경국가공정연구중심소속박오심편공사실험실완성.재료:6월령웅성SD대서6지,체질량(280±20)g.승재환주요성분:유당귀,두중,황기,구기자,록각상,육종용、지별충,수질、단삼,속단등22미중약.유북경시발연제약유한공사제공.방법:6지SD대서채용내독소화갑기강지송룡제주격소성고골두배사동물모형,수궤장대서분위모형조화승재조,매조각3지.승재조대서자제1차주사갑기강지송룡후,관복승재환약액1.5g/kg,1차/d,공관복6주.6주후취고골두제취총RNA,진행기인보측시.주요관찰지표:기인보측시결과중적세포점부분자기인작용로경분석.결과:3지모형대서사용승재환후,여모형대서상비교,출현1.5배이상개변적기인,분별위633개(하조506개,상조127개)、883개(하조640개,상조243개)、593개(하조408개,상조185개).사용MAS연건귀류분석후,공유상관작용로경79개,섭급297개기인.기중세포점부분자로경유8개하조기인.결론:대서복용승재환후,사상술기인하조,회복료대서거서세포급파세포적식별공능,회복료상피세포포괄혈관내피세포적정상생존조건,세포점부분자작용로경지정상수평,저시배사고골두내혈관회복정상혈운적관건.
BACKGROUND: Studies have showed that Chengzai pill is of distinct significance in the treatment of steroid-induced osteonecrosis of femoral head through increasing bone mineral density, bone weight, bone strength and rigidity, it also reverses the low levels of estrogen. OBJECTIVE: To explore the effect of Chengzai pill on the genes of cell adhesion molecules on bone cells of steroid-induced ostaonecrotic rats, and to understand the role to resume normal blood transport in femoral head of steroid-induced osteonecrosis. DESIGN, TIME AND SETTING: Grouping controlled observation was performed in the Pharmacological Laboratory of Wangjing Hospital of China Academy of Chinese Medical Sciences and laboratory of CapitalBio Corporation between March and August in 2006. MATERIALS: Six male SD rats of 6 months old and weighing (280:1:20) g were used in this study. Chengzai pill was consisted of 22 Chinese medicines, such as Chinese Angelica, Eucommia Bark, Milkvetch Root, Barbary Wolfberry Fruit, Degelatined Deer-hom, Desertliving Cistanche, Eupolyphaga seu Steleophaga, Leech, Danshen Root and Himalayan Teasel Root, which were offered by Beijing Boran Pharmaceutical Co., Ltd. METHODS: The lipopolysaccharide and methylprednisolone were applied to prepare a rat model of steroid-induced osteonecrosis of femoral head. Six rats were divided into model group and Chengzai pill group at random with 3 rats in each group. The rats in the Chengzai pill group were administrated with methylprednisolone for the first time and then 1.5 g/kg Chengzai pill solution, once a day, totally for 6 weeks. The total RNA was extracted from femoral head in all rata 6 weeks later and then gene expression profiling was analyzed. MAIN OUTCOME MEASURES: Gene action pathway of cell adhesion molecules in gene expression profile. RESULTS: Compared with model rats, there were totally 8 downregulated genes of cell adhesion molecules which changed by a minimum of 1.5 folds in cell adhesion molecules pathway of Chengzai pill group, three rats were present with 633 genes (506 down-regulated and 127 up-regulated), 883 genes (640 down-regulated and 243 up-regulated) and 593 genes (408 down-regulated and 185 up-regulated), respectively. MAS software classification analysis showed 79 action pathways were involved in 297 genes.CONCLUSION: Following Chengzai pill administration, those downregulated genes recover the cognitive functions of macrophage and target cell in rats, also renew the normal survival condition of epithelial cells including vascular endothelial cells. Cell adhesion molecules action pathway returns to normal levels. This is the key to resume normal blood transport in femoral head of steroid-induced osteonecrosis.