去势小鼠尾静脉注射骨髓间充干细胞通过抑制体内破骨细胞活性治疗绝经后骨质疏松

目的探讨骨髓间充质干细胞(BMMSCs)尾静脉注射对体内破骨细胞活性及骨质疏松治疗作用。方法选用8周龄健康雌性小鼠行双侧卵巢切除术(OVX),建立绝经后骨质疏松模型。选用同一批次、周龄相同、体质量相近的健康小鼠行双侧卵巢附近脂肪组织部分切除,建立假手术组(sham)。对OVX组小鼠尾静脉注射BMMSC治疗,1个月后分别取双侧股骨行TRAP染色及mciro-CT检测体内破骨细胞数量和骨小梁微结构改变。结果 OVX+BMMSC注射组中破骨细胞的数量较OVX不治疗组显著降低。micro-CT显示OVX+BMMSC组骨小梁数量及骨密度显著高于OVX不治疗组。结论尾静脉注射骨髓间充质干细胞能够抑制体内破骨细胞活性,对绝经后骨质疏松具有一定的治疗作用。     

淫羊藿苷调节酸性微环境减轻绝经后老年骨质疏松性疼痛

背景：前期研究已证明，淫羊藿苷在促进骨形成和抑制骨吸收方面具有重要作用，但其对骨质疏松介导的骨痛产生的影响尚未见报道。目的：探讨淫羊藿苷减轻绝经后老年性骨质疏松性骨痛的可能机制。方法：(1)动物实验：将200只C57BL/6小鼠随机分为4组：假手术组、模型组、模型+淫羊藿苷组，模型+碳酸酐酶Ⅱ抑制剂组。除假手术组外，其余各组摘除小鼠卵巢建立绝经后骨质疏松模型。模型+淫羊藿苷组在造模后第2天灌胃淫羊藿苷，每2周进行1次疼痛行为学实验并取材，持续20周。microCT检测股骨骨量、苏木精-伊红染色及TRAP染色检测破骨细胞活性、免疫荧光染色检测神经元形态及相关离子通道表达。(2)细胞实验：提取小鼠骨髓来源的破骨细胞前体细胞，在体外使用RANKL/M-CSF体系诱导分化为破骨细胞并添加不同浓度淫羊藿苷(1,10μmol/L)干预。采用抗酒石酸酸性磷酸酶染色检测破骨细胞分化，采用鬼笔环肽染色检测破骨细胞肌动蛋白环，采用骨板吸收实验检测破骨细胞噬骨功能，采用pH计检测体系pH值，采用Western Blot检测破骨细胞分化相关蛋白表达。此外，提取小鼠背根神经节来源神经细胞并用淫羊藿苷处理，采用C...     

颗粒蛋白前体促进去卵巢小鼠的骨质疏松

目的探讨颗粒蛋白前体(PGRN)对去卵巢小鼠骨质疏松的影响。方法建立野生型和PGRN敲除(PGRN~(-/-))小鼠卵巢切除骨质疏松模型,采用微型计算机断层扫描(Micro-CT)和三维重建获得小鼠骨组织微观结构并进行骨小梁数据分析, HE染色观察骨组织形态,抗酒石酸酸性磷酸酶(TRAP)染色观察骨组织中破骨细胞数量,免疫组织化学染色法检测骨组织核因子κB受体激活蛋白配体(RANKL)、肿瘤坏死因子α(TNF-α)、 P65表达,荧光定量PCR检测骨组织TRAP mRNA水平, Western blot法检测骨组织基质金属蛋白酶9(MMP9)、 MMP14、 P65蛋白水平。结果与野生型小鼠相比, PGRN~(-/-)组小鼠骨密度(BMD)、骨体积分数(BV/TV)、骨小梁数目(Tb.N)及骨小梁厚度(Tb.Th)均显著增加,骨小梁空间距(Tb.S)显著降低;在PGRN~(-/-)小鼠中观察到骨质疏松程度更轻,破骨细胞数量更少,骨组织RANKL、 TNF-α、 P65蛋白, TRAP mRNA, MMP9、 MMP14表达均低于野生型小鼠。结论 PGRN促进卵巢切除小鼠骨质疏松。     

抑制剂BYL719防治卵巢切除致骨质疏松症的研究

目的 PI3K信号通路在破骨细胞前体细胞增殖、破骨细胞分化中均发挥重要功能。BYL719是经典的PI3K通路抑制剂,但其对骨代谢的影响,目前未见报道。方法通过构建卵巢切除后小鼠骨质疏松症模型,运用microCT进行骨组织形态学分析,研究BYL719对骨质疏松症的治疗作用。在此基础上,通过体外研究BYL719对破骨细胞前体细胞活性、破骨细胞分化、破骨细胞特异性基因表达以及破骨细胞骨吸收功能,明确BYL719对破骨细胞的功能。结果 BYL719在5 mg/kg和10 mg/kg浓度下,均可有效防治小鼠卵巢切除导致的骨丢失,可以抑制破骨细胞前体细胞活性,抑制破骨细胞分化以及破骨细胞特异基因表达。结论 PI3K-mTOR抑制剂BYL719可通过影响破骨细胞前体细胞活性、破骨细胞分化,最终达到治疗骨质疏松症的作用。     

补骨脂素对骨质疏松小鼠骨折修复的影响

目的观察补骨脂素对骨质疏松小鼠骨折修复的影响。方法 20只雌性C57BL/6小鼠在建立骨质疏松模型后,随机分为2组:模型组和补骨脂素组,每组10只。所有小鼠在右侧股骨中段建立横形骨折,骨折术后第1天,补骨脂素组按20 mg/kg/d体重量灌胃,每天一次,连续21天,模型组以等剂量生理盐水灌胃。术后21天处死,骨折标本行钼靶X线、组织学和生物力学等检测方法。结果骨折术后第21天,补骨脂素组较模型组骨痂密度变高、骨折线模糊,两组骨痂生成面积比较无明显差异。补骨脂素组软骨细胞数量较模型组明显减少,成骨细胞增生较活跃,软骨骨化形成编织骨。补骨脂素组破骨细胞密度更稀疏,2组中破骨细胞形态和细胞核数量见明显差异。补骨脂素组最大载荷比模型组明显升高。结论补骨脂素作为一种植物雌激素能有效改善骨质疏松小鼠骨痂愈合质量和生物力学性能。     

组蛋白去乙酰化酶在卵巢切除小鼠骨髓间充质干细胞中的表达

背景：骨髓间充质干细胞的多向分化能力在骨代谢疾病中发挥重要作用,受激素、细胞因子等多种因素调节。目前骨髓间充质干细胞骨向分化的表观遗传学调控机制尚不明确,组蛋白去乙酰化酶与骨质疏松的关系尚需进一步探讨。 目的：建立雌激素缺乏骨质疏松小鼠的实验动物模型,检测骨髓间充质干细胞组蛋白去乙酰化酶1,3,4 mRNA表达水平,探索卵巢切除小鼠骨组织形成障碍的表观遗传学机制。 方法：昆明种小鼠30只随机等分为模型组和假手术组。小鼠适应性喂养7 d后,模型组小鼠切除双侧卵巢,造成雌激素缺乏骨质疏松实验动物模型,假手术组小鼠仅切除等量脂肪组织。 结果与结论：模型组小鼠股骨骨小梁稀疏或断裂,骨小梁宽度变窄,骨小梁间距变宽,骨小梁占视野面积降低。与假手术组相比,模型组小鼠骨髓间充质干细胞中组蛋白去乙酰化酶3 mRNA表达水平显著降低,组蛋白去乙酰化酶1,4表达水平变化差异无显著性意义。提示雌激素缺乏导致骨髓间充质干细胞去乙酰化状态改变可能是骨形成障碍的重要原因之一。中国组织工程研究杂志出版内容重点：干细胞;骨髓干细胞;造血干细胞;脂肪干细胞;肿瘤干细胞;胚胎干细胞;脐带脐血干细胞;干细胞诱导;干细胞分化;组织工程全文链接：     

去卵巢大鼠骨组织的变化

目的:观察去卵巢对大鼠骨组织的改变,以建立妇女绝经后骨质疏松的动物模型。方法:选用3月龄SD雌性大鼠16只,随机分为对照组和去卵巢组。去卵巢组大鼠的双侧卵巢被切除,对照组做假手术,持续90天。用骨矿测定仪测量大鼠股骨的骨密度及在半自动图像分析仪观测胫骨近端骨小梁的静、动态指标,并在扫描电镜下观察大鼠股骨松质骨结构的改变。结果:与对照正常组比较,去卵巢组大鼠股骨的远端的骨密度降低(P<0.05)。胫骨骨小梁的面积减少,骨小梁间隙增大。股骨的骨小梁变少,变细,断裂,连接不紧密,表面常见骨吸收形成的陷窝。结论:用切除卵巢的方法造成雌激素缺乏,导致骨质疏松,作为研究因绝经引起的原发性骨质疏松的可靠动物模型。     

去卵巢大鼠骨组织的变化

目的:观察去卵巢对大鼠骨组织的改变,以建立妇女绝经后骨质疏松的动物模型。方法:选用3月龄SD雌性大鼠16只,随机分为对照组和去卵巢组。去卵巢组的大鼠的双侧卵巢被切除,对照组做假手术,持续90天。用骨矿测定仪测量大鼠股骨的骨密度及在半自动图像分析仪观测胫骨近端骨小梁的静、动态指标,并在扫描电镜下观察大鼠股骨松质骨结构的改变。结果:与对照组比较,去卵巢组大鼠股骨远端的骨密度明显降低。胫骨骨小梁的面积减少,骨小梁间隙增加。股骨的骨小梁减少,变细,断裂,连接不紧密,表面常见骨吸收形成的陷窝。结论:用切除卵巢的方法造成雌激素缺乏,导致骨质疏松,是研究因绝经引起原发性骨质疏松的可靠动物模型。     

仙珍骨宝胶囊对去卵巢大鼠股骨颈骨代谢的影响

背景：用骨组织形态计量学方法探讨中药对去卵巢大鼠股骨颈骨质疏松的影响,可为采用中药防治绝经后妇女骨质疏松性股骨颈骨折提供实验依据。 目的：观察仙珍骨宝胶囊对去卵巢大鼠股骨颈松质骨的影响。 方法：3月龄SD雌鼠随机分为4组：基础对照组于实验开始时处死取材,去卵巢组和仙珍骨宝组去卵巢造模,仙珍骨宝组在去卵巢后灌胃仙珍骨宝,去卵巢组和年龄对照组灌胃生理盐水,90 d后处死,取股骨颈经不脱钙骨制片进行骨组织形态计量学参数测量。 结果与结论：与年龄对照组比较,去卵巢大鼠静态参数的骨小梁面积百分数和骨小梁数量明显减少(P < 0.01),骨小梁间隙明显增大(P < 0.01);动态参数的每毫米破骨细胞数和破骨细胞贴壁表面长度明显增加(P < 0.01),骨矿化沉积率明显减少(P < 0.01)。说明去卵巢能导致大鼠股骨颈骨量显著减少。给予仙珍骨宝治疗后,大鼠的骨小梁厚度及骨小梁面积明显增加(P < 0.05),每毫米破骨细胞数和破骨细胞贴壁表面长度有所减少,标记周长百分数则有所增加。说明仙珍骨宝能阻止去卵巢所致的大鼠股骨颈骨量丢失。     

耐力运动对青年与老年小鼠股骨组织微结构变化的影响

目的　应用原子力显微镜（atomic force microscope,AFM）观察中等强度耐力运动后青年与老年小鼠股骨组织微结构的变化,并探讨耐力运动对预防和改善骨质疏松的适宜年龄阶段。 方法　不同月龄清洁级雄性C57小鼠40只,平均分为3月龄青年组和16月龄老年组,每组再平均分为对照组和运动组。青年及老年运动组使用转棒仪跑步运动12周,运动参数15 r/min,25 min/日。对照组正常饲养。实验结束后处死各组小鼠取股骨,石蜡包埋切片后通过AFM观察小鼠股骨皮质骨组织微结构。 结果　青年对照组可见骨陷窝环绕哈弗系统排列规则,有骨小管与其相沟通,钙磷晶体部分呈小柱状,部分呈团状分布;与青年对照组相比青年运动组可见骨陷窝数量及大小变化,表面粗糙度显著降低（P＜0.05）,提示骨组织表面平滑度增加,骨量增加;与青年对照组相比老年对照组可见骨陷窝数量大小变化,钙磷晶体数量减少,表面粗糙度显著增高（P＜0.05）,提示存在骨质疏松;与老年对照组相比老年运动组可见骨陷窝及钙磷晶体数量及大小无明显改变,表面粗糙度改变无统计学意义。 结论　中等强度耐力运动可以改善青年小鼠骨组织微结构,提高骨质量,但对已经发生骨质疏松的老年小鼠骨微结构无明显改善。提示老年骨质疏松的运动预防可能需要从成年开始。     

氯化锂对去卵巢骨质疏松大鼠骨微结构和骨髓基质细胞分化的影响

背景：骨质疏松是一种好发于绝经后妇女的慢性骨代谢疾病,随着世界人口老龄化的增加,如何预防和治疗绝经后骨质疏松是目前困扰医疗界的一大难题。 目的：探讨氯化锂对去卵巢骨质疏松大鼠骨微结构和骨髓基质细胞分化的影响。 方法：将30只3月龄雌性健康未孕SD大鼠去卵巢,因2只大鼠由于感染死亡,将剩下28只大鼠随机分为去卵巢体内组(9只)、去卵巢体外组(10只)和氯化锂组(9只)。手术后第11周,氯化锂组按照体质量每周腹腔注射3次氯化锂,剂量为15 mg/kg,干预8周后,用micro-CT检测9只去卵巢体内组和9只氯化锂组大鼠左侧股骨的骨微结构。10只去卵巢体外组大鼠的双侧股骨和胫骨用于骨髓基质细胞的培养,接种24 h后加入氯化锂,分为0 mmol/L(对照组)、1 mmol/L组和5 mmol/L组,培养至第6天和第8天更换培养基并加入相应浓度氯化锂,培养第10天处理细胞,用Western blot检测其SP7、Runx2和PPARγ2蛋白的表达水平。 结果与结论：①体内结果表明,氯化锂组体积骨密度、骨体积分数和骨小梁数目显著高于去卵巢体内组,骨小梁间隙显著低于去卵巢体内组,而骨小梁厚度和结构模型指数无显著变化。②体外结果表明,1 mmol/L和5 mmol/L氯化锂组骨髓基质细胞Sp7和Runx2蛋白表达水平显著高于对照组,而PPARγ2蛋白表达水平显著低于对照组。③以上实验结果表明,氯化锂可能是通过促进去卵巢骨质疏松大鼠骨髓基质细胞向成骨分化而改善去卵巢骨质疏松大鼠的骨微结构。中国组织工程研究杂志出版内容重点：干细胞;骨髓干细胞;造血干细胞;脂肪干细胞;肿瘤干细胞;胚胎干细胞;脐带脐血干细胞;干细胞诱导;干细胞分化;组织工程     

雷公藤甲素通过抑制破骨细胞生成预防骨丢失的研究

目的 探讨雷公藤甲素抗骨质疏松的作用及机制。方法 建立大鼠老年性骨质疏松模型。40只22月龄雄性SD大鼠随机分为雷公藤甲素（每天15μg/kg腹腔注射）治疗组和生理盐水对照组（每天15μg/kg腹腔注射）,连续8周。采用显微CT分析胫骨近端骨松质的骨密度(BMD)和骨显微结构。WB检测成骨相关蛋白表达水平。TRACP-5b染色法测定破骨细胞数,同时检测骨吸收标志物表达水平。结果 显微CT结果显示,雷公藤甲素治疗组大鼠骨密度、骨体积/总体积比值(Bv/Tv)、骨小梁厚度(Tb.Th)、骨小梁数目(Tb.N)、骨小梁间距(Tb.Sp)均显著高于对照组（P<0.05）。两组的成骨相关蛋白表达水平无明显差异,TRACP-5b染色显示雷公藤甲素减少了体内破骨细胞的数量（P<0.05）,同时血液骨吸收标志物水平也明显降低（P<0.05）。结论 雷公藤甲素通过抑制破骨细胞生成进而对老年性骨质疏松有保护作用。雷公藤甲素可能是治疗老年性骨质疏松症的一种可行方案。     

Effect of 16,16-dimethyl prostaglandin E2 methyl ester on weanling rat skeleton: daily and systemic administration

The effects of 0, 0.3, 1.0, and 3.0 mg of 16,16-dimethyl prostaglandin E2 methyl ester (Di-M-PGE2) per kilogram per day administered subcutaneously for 21 days to fluorescent-labeled weanling rats were studied, by single-photon absorptiometric and static and dynamic histomorphometric techniques, to determine possible alterations in growth and mineralized tissue mass and their mechanisms of response. Specimens of femurs, proximal tibia, and tibial shaft were analyzed. Di-M-PGE2 caused a reduction in bone elongation and a dramatic accumulation in metaphyseal trabecular hard tissue mass. At high doses, the growth cartilage exhibited reduced thickness and degenerative cell size and cell production rate. The increased metaphyseal trabecular hard tissue mass was restricted to the secondary spongiosa region and was observed at all dose levels. The metaphysis was further characterized by an increase in bone and calcified cartilage cores, a marked elevation in osteoblast and osteoclast numbers, in osteoblast-to-osteoclast ratios, and in ratios of differentiated cells to osteoprogenitor cells. These findings were consistent with the interpretations that Di-M-PGE2 depressed bone elongation by delaying the division and maturation of growth plate chondrocytes; stimulated the differentiation of osteoblasts and osteoclasts, thus generating more differentiated bone cells but suppressing their activities; and increased metaphyseal trabecular hard tissue by creating an imbalance in osteoblasts over osteoclasts and suppressing hard tissue resorption.     

Prevention of Osteoporosis in Mice after Ovariectomy via Allograft of Microencapsulated Ovarian Cells

It is believed that estrogen deficiency is one of the major risk factors associated with osteoporosis. To investigate the effects of the transplantation of microencapsulated ovarian cells in estrogen‐deficient mice, ovarian cells from female Kunming (KM) mice (6‐weeks old) were separated, cultured, and microencapsulated with alginic acid‐polylysine‐alginic acid. Female KM mice (8‐weeks old) were randomly separated into three groups: intact (normal), ovariectomized (OVX), and treatment (OVX+ implantation). Microencapsulated ovarian cells were found to secrete estrogen at normal levels in vitro. Ninety days after transplantation, serum estradiol levels in the OVX group were significantly lower, and the trabecular bone amount and volume were decreased when compared with the normal group. The expression of alkaline phosphatase in chondrocytes appeared lower, while the expression of matrix metalloproteinase 9 (MMP‐9) in the bone matrix was higher. The ratio of MMP‐9‐positive chondrocytes and osteoblasts to osteoclasts was significantly lower than that of the normal group. The concentrations of hydroxyproline (Hyp), Ca, and P in the left femurs of the OVX group were lower than those of the normal group. However, the aforementioned changes were not seen in the treatment group. In conclusion, microencapsulated ovarian cells survive well after transplantation and secrete estrogen in vivo, and they can prevent in some degree osteoporosis caused by ovariectomy. Anat Rec, 2010. © 2009 Wiley‐Liss, Inc.     

仙灵骨葆对尾悬吊拟失重大鼠骨量丢失的抑制

背景：以淫羊藿苷为主要成分的中药制剂仙灵骨葆具有促进骨形成的作用。 目的：观察仙灵骨葆对尾悬吊拟失重大鼠骨量丢失的抑制作用及机制。 方法：将SD大鼠随机分为正常对照组、拟失重组、仙灵骨葆组,后两组大鼠采用尾悬吊法模拟失重,仙灵骨葆组悬吊同时灌胃给予仙灵骨葆250 mg/(kg•d),拟失重组悬吊同时灌胃给予双蒸水,4周后取右侧股骨行骨密度、三点弯曲生物力学及骨组织形态计量学检测。 结果与结论：正常对照组骨密度、胫骨近端骨小梁相对体积、骨小梁厚度、骨小梁数量、生物力学最大载荷显著高于拟失重组、仙灵骨葆组(P < 0.05)。仙灵骨葆组胫骨远端1/4骨密度、胫骨近端骨小梁相对体积显著高于拟失重组(P < 0.05),生物力学最大载荷也高于拟失重组,但差异无显著性意义。说明仙灵骨葆灌胃干预可促进松质骨的骨形成,部分阻止拟失重大鼠骨量的丢失。      

Adenosine A(2A) receptor ligation inhibits osteoclast formation

Adenosine is generated in increased concentrations at sites of injury/hypoxia and mediates a variety of physiological and pharmacological effects via G protein-coupled receptors (A(1), A(2A), A(2B), and A(3)). Because all adenosine receptors are expressed on osteoclasts, we determined the role of A(2A) receptor in the regulation of osteoclast differentiation. Differentiation and bone resorption were studied as the macrophage colony-stimulating factor-1-receptor activator of NF-κB ligand formation of multinucleated tartrate-resistant acid phosphatase (TRAP)-positive cells from primary murine bone marrow-derived precursors. A(2A) receptor and osteoclast marker expression levels were studied by RT-PCR. Cytokine secretion was assayed by enzyme-linked immunosorbent assay. In vivo examination of A(2A) knockout (KO)/control bones was determined by TRAP staining, micro-computed tomography, and electron microscopy. The A(2A) receptor agonist, CGS21680, inhibited osteoclast differentiation and function (half maximal inhibitory concentration, 50 nmol/L), increased the percentage of immature osteoclast precursors, and decreased IL-1β and tumor necrosis factor-α secretion, an effect that was reversed by the A(2A) antagonist, ZM241385. Cathepsin K and osteopontin mRNA expression increased in control and ZM241385-pretreated osteoclasts, and this was blocked by CGS21680. Micro-computed tomography of A(2A)KO mouse femurs showed a significantly decreased bone volume/trabecular bone volume ratio, decreased trabecular number, and increased trabecular space. A(2A)KO femurs showed an increased TRAP-positive osteoclast. Electron microscopy in A(2A)KO femurs showed marked osteoclast membrane folding and increased bone resorption. Thus, adenosine, acting via the A(2A) receptor, inhibits macrophage colony-stimulating factor-1-receptor activator of NF-κB ligand-stimulated osteoclast differentiation and may regulate bone turnover under conditions in which adenosine levels are elevated.     

Histologische Charakteristika und Häufigkeit der sekundären Osteoporose bei systemischer Mastozytose Eine retrospektive Analyse an 158 Fällen

Mastocytosis is characterized by abnormal proliferation of mast cells especially within the skin and bone marrow and is often associated with osteoporosis. Mast cells can synthesize a variety of cytokines that are known to affect the skeletal system, but the cellular and pathophysiological mechanisms leading to osteoporosis in systemic mastocytosis remain poorly understood. To further characterize mastocytosis-associated osteoporosis we compared bone histomorphometric findings in iliac crest biopsy specimens from 158 untreated patients with mastocytosis. The overall prevalence of mastocytosis in the specimens diagnosed with osteoporosis was 1.25%, but that in patients younger than 45 years was 2.25%. The male-to-female ratio was 1:1, in contrast to 1:2 in osteoporosis. Osteopenia was present in 64% of the patients with mastocytosis, while osteosclerosis was rare (3%). Histological criteria are the concentric increase in mast cells in the perivascular tissue and the increase in elongated mast cells within the marrow space. Histomorphometry showed mastocytosis to be associated with moderate hyperosteoidosis and increased perforating bone resorption, indicated by a significant decrease in bone volume, trabecular thickness, and trabecular number as compared to controls. Osteoclast number was not altered, pointing to a functional effect of mast cells and/or its product on osteoclasts, rather than an effect on osteoclast differentiation. We conclude that although the prevalence of mastocytosis seems to be low, its correct and early diagnosis is crucial for at least 2.25% of younger patients with osteoporosis.     

脂肪源干细胞移植骨质疏松模型大鼠骨密度及骨形态计量学指标的变化

BACKGROUND:Stem cell transplantation is increasingly hoped to promote osteoblast differentiation and inhibit osteoclast proliferation in the treatment of osteoporosis. OBJECTIVE:To study the therapeutic effect of exogenous adipose-derived stem cell (ADSC) transplantation on osteoporosis in ovariectomized rats. METHODS:Thirty Sprague-Dawley female rats were equivalently randomized into sham, model, ADSC transplantation groups. Rats in all groups except the sham group underwent bilateral ovariectomy to make osteoporosis models. Surrounding adipose tissues instead of the ovary were removed in the sham group. After modeling, rats were given 2×10⁶ ADSCs at passage 4 via the tail vein in the transplantation group and the same volume of normal saline in the model group, once a week. After 6 weeks, levels of serum calcium, phosphorus, and alkaline phosphatase as well as bone mineral density and histomorphometry indicators were detected in rats. RESULTS AND CONCLUSION:Compared with the sham group, the trabecular bone volume fraction was significantly decreased in the model group (P < 0.01), but remarkably increased after ADSC transplantation (P < 0.05). After modeling, the bone trabecular absorption surface percentage and rate of bone trabecular formation were elevated significantly (P < 0.05 or P < 0.01), while these increases were improved by ADSC transplantation (P < 0.05). Additionally, the levels of serum calcium and alkaline phosphatase and bone mineral density were significantly decreased after modeling, but were increased after ADSC transplantation. In contrast, the serum level of phosphorus was significantly increased in the model group (P < 0.05) but decreased markedly in the ADSC transplantation group (P < 0.05). To conclude, ADSC transplantation can reduce the loss of bone mass in osteoporosis rats by ovariectomy.     

Runx2，Osterix 及MMP-13在大鼠激素性股骨头无菌性坏死组织中的表达及意义

目的　探讨Runx2,Osterix及MMP-13蛋白及基因在大鼠激素性股骨头无菌性坏死组织中的表达。 方法　40只成年Wistar大鼠随机分为模型组（30只）和对照组（10只）。模型组大鼠接受地塞米松20 mg/kg肌肉注射,1次/周,注射后,在跑步机上对动物进行训练。模型组根据训练时间分为3组（各10只）：A组8周;B组10周;C组12周。采用PCR和Western blot方法检测大鼠股骨头组织中基因及蛋白变化。 结果　模型组大鼠脂肪细胞最大直径、空骨陷窝率高于对照组,且随着训练时间的增加,脂肪细胞最大直径、空骨陷窝率逐渐增加,差异具有统计学意义（P<0.00）;模型组骨小梁面积低于对照组,且随着训练时间的增加,骨小梁面积逐渐降低,差异具有统计学意义（P<0.00）。模型组大鼠Runx2,Osterix蛋白与基因表达量低于对照组,且随着时间的延长,表达量逐渐降低,差异具有统计学意义（P<0.05）。模型组大鼠MMP-13蛋白与基因表达量高于对照组,且随着时间的延长,表达量逐渐增加,差异具有统计学意义（P<0.05）。 结论　激素性股骨头坏死组织中Runx2,Osterix在mRNA和蛋白表达水平均低于正常股骨头组织,MMP-13高于正常股骨头组织。