抗骨松颗粒对去卵巢大鼠骨质含量和生物力学的影响

目的 探讨抗骨松颗粒对去卵巢大鼠骨质疏松模型骨质含量和骨生物力学性能的影响.方法 40只10月龄Wistar雌性大鼠随机分为对照组、模型组、抗骨松组和倍美力组,每组10只.正常对照组做假手术,其余3组做卵巢切除术.术后3个月开始给药,连续用药满90 d,处死动物,取出第2腰椎和股骨,测定骨密度、钙、磷、锰、镁、羟脯氨酸、碱性磷酸酶和有机质含量;取出第3腰椎,测骨质含量和生物力学性能.结果 抗骨松颗粒能明显提高骨质疏松大鼠的骨密度、钙、锰、镁、羟脯氨酸和有机质含量,增强腰椎骨的抗压生物力学性能.结论 应用抗骨松颗粒可以明显改善去卵巢大鼠骨质疏松模型骨质含量和骨的生物力学性能.     

密骨胶囊对去卵巢大鼠骨质疏松模型的影响

目的 探讨密骨胶囊对去卵巢骨质疏松模型大鼠腰椎整体骨量和骨质成分丢失的影响。方法 40只10月龄Wistar雌性大鼠随机分为正常组、模型组、密骨胶囊组和倍美力组,每组10只。正常组仅行假手术,其余三组行卵巢切除术。术后91天开始给药,连续用药满90天,处死,取出第2腰椎,测定整体骨量和钙、磷、有机质含量。结果 密骨胶囊能明显提高骨质疏松大鼠腰椎骨的整体骨量和钙、磷、有机质含量。结论 密骨胶囊能增强骨质疏松大鼠腰椎的骨量,改善骨结构。     

健骨二仙提取液对去卵巢大鼠骨形态计量学的影响

将42只6．5月龄雌性Wistar SPF级近交系大鼠随机分为4组,假手术组11只,单纯卵巢切除手术组10只,卵巢切除＋健骨二仙提取液治疗组11只,卵巢切除＋倍美力治疗组10只,采用去卵巢方法进行骨质疏松造模。全部处死大鼠后,取右胫骨上段不脱钙骨切片进行骨形态计量学静态及动态参数分析。结果显示,健骨二仙提取物对大鼠胫骨上段松质骨的静态学参数及动态学参数均有良好的改善作用,可抑制去卵巢后高转换型骨质疏松的形成。     

长期有氧运动对去卵巢大鼠骨组织中内源性硫化氢生成的影响

目的探讨长期有氧运动对去卵巢大鼠骨组织中内源性硫化氢生成的影响。方法实验分为三组:假手术组,骨质疏松模型组(去卵巢组),去卵巢+运动组(运动组)。运动为跑台运动,持续12 w。结果经过长期有氧运动之后,去卵巢组大鼠股骨骨密度(BMD)和骨矿物质含量明显增加;股骨极限负荷和刚度明显增加,血浆硫化氢水平明显增加;股骨中胱硫醚β合酶和胱硫醚γ分解酶表达水平明显上调;血浆丙二醛(MDA)含量明显降低(均P0.05);3-疏基丙酮酸硫基转移酶变化差异无统计学意义(P0.05)。结论长期有氧运动增加去卵巢大鼠骨组织中内源性硫化氢的生成,从而减轻氧化应激,最终有助于减轻去卵巢大鼠的骨质丢失。     

强骨宝对去势大鼠骨形态计量学影响的研究

目的 观察强骨宝（黄芪＋司坦唑醇,JGB）对去卵巢大鼠骨质疏松症骨形态计量学参数的影响.方法 取32只Wistar雌性大鼠随机分为4组,行去势手术,制成去卵巢大鼠骨质疏松模型.然后分别灌胃给药生理盐水、己烯雌酚、强骨宝,8 w后处死,取大鼠胫骨上段松质骨和中段皮质骨硬组织包埋、切片,图像分析松质骨、皮质骨形态计量学参数.结果 强骨宝可使去卵巢大鼠松质骨静态参数和动态参数显著增加,吸收参数显著降低;皮质骨面积、骨髓腔面积等静态及内外骨膜骨形成动态参数均无显著变化,内膜面骨吸收参数降低.结论 强骨宝能有效预防去卵巢大鼠骨质疏松症松质骨丢失,亦具有抑制皮质骨内膜骨吸收的作用.     

活性维生素D3对去卵巢骨质疏松大鼠骨质量、维生素D代谢物水平及肾脏维生素D受体(VDR)mRNA表达的影响

目的 研究活性维生素D3对去卵巢骨质疏松大鼠骨质量25(OH)D3和1,25(OH)2D3水平及肾脏VDR mRNA表达的影响,为临床防治骨质疏松提供依据.方法 36只八月龄健康雌性SD大鼠随机分为3组,即模型组(Model),假手术组(Sham),活性维生素D3治疗组(Treatment),每组12只,对照治疗三月后全部处死,用双能X线骨密度仪及生物力学技术评估模型的骨密度及骨质量,采用酶联免疫吸附方法检测血清或组织中25(OH)D3和1,25(OH):D3含量,用FQ-PCR方法检测肾脏组织中VDR mRNA的表达情况.结果 (1)模型大鼠股骨头及粗隆部的BMD及骨生物力学指标(最大载荷和最大压应变)均明显下降(P<0.05);(2)活性维生素D3治疗组与模型组比较,血清、肝脏和肾脏组织中25(OH)D3和1,25(OH)2D3的含量明显提高(P<0.05),与假手术组比较无统计学意义;(3)模型组大鼠肾脏VDR mRNA的表达显著低于活性维生素D3治疗组(P=0.004).结论 本实验结果提示适当补充活性维生素D3可有效的防治去卵巢大鼠骨量丢失和骨质量下降,为临床活性维生素D应用提供实验依据.     

去卵巢所致骨质疏松大鼠骨压缩与冲击力学性能实验研究

目的研究正常鼠和去卵巢所致骨质疏松大鼠骨的压缩、冲击力学性质。方法选用280~320g,10月龄Wistar雌性大鼠20只,随机分为正常对照组10只,模型组10只。对模型组大鼠于0w摘除其卵巢。正常对照组和模型组大鼠饲养14w后,以腹主动脉放血法处死大鼠。取大鼠股骨进行压缩实验,取大鼠胫骨进行冲击实验。结果得出了大鼠股骨压缩力学性能指标和大鼠胫骨冲击力学性能指标。结论模型组压缩和冲击力学性能指标显著降低。     

艾灸防治绝经后骨质疏松的实验研究

目的观察艾灸对可造成卵巢切除大鼠骨质疏松的各项指标的影响,探讨艾灸对绝经后妇女骨质疏松的治疗作用。方法将30只大鼠随机分为对照组、模型组、艾灸组,每组10只。除正常对照组外,其余两组大鼠摘除双侧卵巢。3 d后对艾灸组经行治疗,三组均正常摄食饮水,之后观察并测定每组大鼠血清雌二醇(E2)、骨钙素(BGP)含量及尿Ca、肌酐(Cr)的含量。结果卵巢切除的模型组与正常对照组相比血清E2明显下降(P<0.05);艾灸组治疗后与模型组比较E2水平有显著差异(P<0.05),与正常对照组E2水平没有显著差异(P>0.05);艾灸组的血清骨钙素明显高于模型组与对照组。尿钙与肌酐的比值艾灸组明显低于模型组(P<0.05),而与正常对照组比较差异无统计学意义。结论艾灸对骨质疏松症具有明显的防治作用,值得临床应用推广。     

运动训练对去卵巢大鼠生物力学性能及骨代谢指标的影响

目的探讨运动训练对去卵巢大鼠生物力学性能及骨代谢指标的影响。方法选取30只雌性SD大鼠,按照随机数字表法分为正常对照组、模型对照组、运动组,每组10只,其中模型对照组、运动组进行去卵巢处理,正常对照组仅取出卵巢周围的脂肪组织。建模成功后正常对照组、模型对照组大鼠在笼内自由活动,而运动组大鼠给予适当的运动训练。在运动训练结束后对比3组大鼠的骨密度(BMD)、骨矿物质含量(BMC)、股骨生物力学性能指标、血清Ca、血清P、抗酒石酸酸性磷酸酶(STR-ACP)、骨钙素(BGP)含量。结果正常对照组BMD和BMC显著高于模型对照组,BMD显著高于运动组(均P0.05)。运动组BMD高于模型对照组(P0.05)。运动组最大荷载、弹性荷载、破坏载荷、刚性系数、能量吸收显著高于正常对照组和模型对照组(均P0.05)。正常对照组最大荷载、弹性荷载、能量吸收显著高于模型对照组(P0.05)。运动组血清Ca含量明显低于正常对照组和模型对照组,而正常对照组血清Ca含量明显低于模型对照组(均P0.05);运动组血清P含量明显高于正常对照组和模型对照组,正常对照组血清P含量明显低于模型对照组(均P0.05);模型对照组血清STR-ACP含量明显高于运动组和正常对照组,运动组血清STR-ACP含量明显高于正常对照组(P0.05);模型对照组血清BGP含量显著低于正常对照组和运动组(均P0.05)。结论运动训练能明显提高去卵巢大鼠BMD,增强股骨生物力学性能,改善骨代谢指标,有利于降低骨质疏松症的发生率。     

小剂量17β雌二醇对去卵巢大鼠松质骨的作用

10月龄SD大鼠200只分为3组：去卵巢大鼠；去卵巢大鼠17β雌二醇干预组；假手术组。发现小剂量17β雌二醇对卵巢切除所致的松质骨丢失有防治作用。     

补肾中药复方对去卵巢骨质疏松大鼠皮质骨生物力学性能的改善作用及机制的实验研究

目的　探讨补肾中药复方对去卵巢骨质疏松模型大鼠皮质骨 (股骨 )生物力学性能的作用及其相关的机制。方法　将 50只 1 0月龄Wistar雌性大鼠随机分为 5组 ,每组 1 0只。正常对照组做假手术 ,其余 4组做卵巢切除术。术后正常饲养 90 d,第 91天开始给药 ,连续用药 90 d,处死 ,测定股骨的骨矿密度、几何尺寸和股骨的生物力学性能。结果　模型大鼠股骨的生物力学性能明显下降 ,骨强度降低 ;股骨干外径变细 ,股骨中段骨皮质面积减少 ,骨矿密度有所下降。补肾中药复方组 (密骨胶囊组和仙灵骨葆组 )大鼠股骨的生物力学性能明显提高 ,骨强度增加 ;股骨中段外径增粗 ,骨皮质面积增加 ,骨矿密度提高。结论　补肾中药复方通过提高去卵巢骨质疏松模型大鼠皮质骨 (股骨 )的宏观结构生物力学应答机能 ,明显改善其生物力学性能。     

仙灵骨葆改善骨质疏松大鼠股骨骨生物力学性能的作用及机制研究

目的探讨补肾中药仙灵骨葆对去卵巢骨质疏松模型大鼠皮质骨(股骨)生物力学性能的作用及其相关的机制。方法将40只10月龄wistar雌性大鼠随机分为仙灵骨葆组、倍美力组、正常组和模型组,每组10只。正常组做假手术,其余3组做卵巢切除术。术后正常饲养90 d。第91天开始,仙灵骨葆组、倍美力组分别给予临床等效剂量相应药物:仙灵骨葆55 mg/d(胶囊量),倍美力0.01 mg/d,正常组和模型组不给药。连续给药90 d后处死大鼠,测定股骨的几何尺寸、极惯性矩、抗扭截面模数、截面惯性矩、抗弯截面模数、骨矿密度和股骨的生物力学试验。结果模型大鼠股骨干外径变细,骨皮质面积减少,抗弯、抗扭截面模数变小,骨矿密度减损;股骨的生物力学性能明显下降,骨强度降低。用药组大鼠股骨干外径增粗,骨皮质面积增加,抗弯、抗扭截面模数增大,骨矿密度提高。股骨的生物力学性能明显改善,骨强度增加。结论仙灵骨葆能够提高股骨宏观结构的生物力学应答调节功能,使股骨干外径增粗,皮质骨面积增加,骨丢失减少使股骨结构的抗弯、抗扭截面模数增大,使骨的力学结构优化,骨强度提高。     

补肾活血方对去势大鼠骨质疏松的影响

目的观察补肾活血方对去势大鼠的血生化、骨密度、生物力学及病理学的影响,评价补肾活血方防治去势大鼠骨质疏松的疗效。方法取36只雌性大鼠随机分为对照组、假手术组和补肾活血组。补肾活血组与对照组大鼠行卵巢切除术,假手术组行假手术处理,均饲养3个月后行病理检查确认造模成功。造模成功后各组大鼠分别给予0．9％氯化钠注射液、0．9％氯化钠注射液、补肾活血中药灌胃,3个月后处死取血分离得到血清,分别检测血清雌激素（E：）、碱性磷酸酶（ALP）和骨钙素（BGP）。取大鼠腰椎、股骨测量腰椎的骨密度（BMD）和最大承载力、行股骨病理学观察。结果与对照组比较,补肾活血方组大鼠血清E：升高,差异有统计学意义（P〈0．01）;骨形成指标ALP、BGP上升,差异有统计学意义（P〈0．05）。与对照组比较,补肾活血组大鼠腰椎BMD及最大承载力均升高,差异有统计学意义（P〈0．05）。HE染色病理组织形态观察发现补肾活血方组大鼠骨小梁稍细,无明显变薄,排列尚整齐并连接成网,密度、面积尚正常,部分区域骨小梁间隙略增大,较对照组有明显改善。结论补肾活血方能够提高去势大鼠雌激素水平,促进骨形成,增加骨量,提高骨组织的力学性能,改善骨组织状况,达到防治骨质疏松的疗效。     

叶酸对去卵巢大鼠骨质疏松的保护作用

目的 探讨叶酸对去卵巢大鼠骨质疏松的保护作用.方法 40只3月龄雌性SD大鼠随机分为5组:假手术组、去卵巢组、乙烯雌酚组(乙烯雌酚0.03 mg·kg-1·d-1)、低剂量叶酸组(叶酸5 mg·kg-1·d-1)、高剂量叶酸组(叶酸20 mg·kg-1·d-1).各组大鼠于术后1周开始灌胃给药,治疗10周,假手术组和去卵巢组给予溶媒灌胃.测定大鼠血浆总同型半胱氨酸(tHcy)浓度,骨匀浆中碱性磷酸酶(ALP)和抗酒石酸酸性磷酸酶(TRACP)的水平;取右股骨和腰5椎体进行骨密度和骨生物力学测定,取腰6椎体和左股骨制备HE切片,观察骨组织的形态学变化.结果 与假手术组比较,去卵巢大鼠血浆tHcy浓度明显升高,腰椎和股骨骨密度显著减低(均P＜0.01),血浆tHcy浓度与腰椎骨密度呈负相关(r=-0.359,P=0.040).叶酸显著降低去卵巢大鼠血浆tHcy浓度(均P＜0.01).大剂量叶酸显著增加去卵巢大鼠骨匀浆ALP水平,降低TRACP水平,增加腰椎和股骨骨密度(均P＜0.01),改善腰椎和股骨的生物力学性能.结论 去卵巢大鼠存在高同型半胱氨酸血症,高同型半胱氨酸参与了去卵巢大鼠骨质疏松的发生.叶酸对去卵巢大鼠骨质疏松具有保护作用,其机制可能与改善同型半胱氨酸的代谢作用有关.

Abstract：

Objective To investigate the protective effect of folic acid(FA) on osteoporosis in ovariectomized(OVX) rats.Methods Forty three-month-old female SD Rats were divided into 5 groups, sham operation group, OVX group, diethylstilbestrol group(0.03mg·kg-1·d-1),low dose FA Group (5 mg·kg-1·d-1),and high dose FA group (20 mg·kg-1·d-1).Gastric gavage in each group was started from one week after being ovariectomized and lasted 10 weeks. Sham operation group and OVX group were treated with solvent. The rats were sacrificed at the end of 10th week after treatment. The total homocysteine(tHcy) in plasma, alkaline phosphatase(ALP), and tartrate-resistant acid phosphatase(TRACP) activity of bone homogenates were measured. The bone mineral density(BMD) and bone biomechanics were determined using L5 vertebrae and right femur. The bone tissue slices were made with L6 vertebrae and left femur and HE stained, and then the histomorphology was observed. Results Compared with sham operation group, plasma tHcy level was significantly increased(P＜0.01), BMD of lumbar vertebrae and femur was remarkedly decreased in OVX group(all P＜0.01). Plasma tHcy concentration was negatively correlated with lumbar BMD(r=-0.359, P=0.040). Plasma tHcy level in both groups treated with folic acid was significantly reduced(all P＜0.01). The ALP concentration in bone homogenates was higher, the TRACP concentration in bone homogenates was lower, and BMD and bone biomechanics of lumbar vertebrae and femur were increased in high dose FA group than those in OVX group(all P ＜0.01). Conclusions In OVX rats hyperhomocysteinemia existed and was involved in the development of osteoporosis. Folic acid could protect OVX rats from osteoporosis, due probably to improved homocysteine metabolism.     

IGF-1对去卵巢大鼠骨密度及骨力学强度的影响

目的 研究外源性胰岛素样生长因子-1(IGF-1)对去卵巢(OVX)骨质疏松大鼠骨密度、骨转换率、骨力学强度等方面的影响.方法 对大鼠施行双侧卵巢摘除术,术后3个月以骨密度测定证实骨质疏松的存在后,随机分为5组,分别以生理盐水、甲状旁腺激素1-34及3种不同剂量IGF-1进行干预.同时设立生理盐水干预的假手术大鼠作为对照.8周后检测血清钙、磷、骨钙素水平及碱性磷酸酶活性;测定腰椎骨密度、股骨力学强度;组织学染色测定股骨远端骨皮质厚度.结果 IGF-1虽未提高OVX大鼠腰椎骨密度却可以显著提高其股骨力学强度.血清学检测结果表明,IGF-1可降低血清钙、磷、骨钙素水平及碱性磷酸酶活性;组织学染色显示IGF-1可显著提高OVX大鼠股骨骨皮质厚度.结论 IGF-1可增加OVX大鼠股骨的力学强度,此作用可能是通过改善骨结构而非提高骨密度所实现的.     

依普拉芬和雌激素对去势后雌性大鼠骨丢失的影响

目的为了探讨依普拉芬对绝经后骨质疏松的防治作用。方法 以去势后雌性大鼠作实验模型,双能Ｘ线吸收骨密度测定（ＤＥＸＡ）及光镜图像分析方法,观察依普拉芬对去势后雌性大鼠骨丢失的作用及单独同期联合和交替使用雌激素,依普拉芬对椎骨、股肌骨密度的影响。结果 依普拉芬与去势组间骨密度有显著性差异,各用药组之间无显著性差异;光镜图像分析示去势组与依普拉芬组及其他各组间均有显著性差异。依普 分组与正常组间无显著性     

Neonatal treatment with sex steroids: relationship between the uterotropic response and the estrogen "receptor" in prepubertal rats.

We tested the hypothesis that neonatal treatment of rats with testosterone propionate (TP) or estradiol benzoate (EB) reduces the uterine responsiveness to estradiol and reduces the concentration of estrogen "receptor" before puberty, and that both of these events precede the onset of the persistent estrus syndrome. Thre-day-old female rats were injected with 100 mug EB, TP or sesame oil (controls) and at 23 and 31 days of age (before the onset of puberty) the uterine cytoplasmic content of specific 8S estradiol-binding protein was measured by sucrose density gradients. Binding by the nuclear fraction was also measured utilizing an exchange assay. In a subgroup of rats also treated neonatally, 2 mug/kg body weight estradiol-17beta was injected at 22 and 30 days of age and uterine wiights were measured as a test for uterine responsiveness. At 23 and 31 days of age the uterine cytoplasmic 8S estrogen "receptor" was significantly reduced in the EB-treated rats, but the uterotropic response to estradiol was blocked only in the 23 day old rats; the uterine response at 31 days was slightly, but not significantly, reduced. In contrast, neonatally administered TP had no effect on either the concentration of cytoplasmic estradiol-binding sites or uterine responsiveness. Nuclear binding of estradiol was unaffected by either TP or EB treatment in both age groups. In a futher experiment in rats ovariectomized at 9 days of age, those treated neonatally with EB had significantly smaller uteri than their untreated ovariectomized controls, thus providing indirect evidence for an extravarian factor affected by neonatal treatment. These data support the hypothesis that neonatal EB treatment may directly inhibit the synthesis or replenishment of the 8S estradiol "receptor" prior to the development of the persistent estrus syndrome (persistent vaginal estrus, anovulation and polycystic ovaries). A neonatally-induced neuroendocrine disorder affecting steroid secretion by the ovary or adrenal may also exist prepubertally to account for the uterine defects.     

Ovariectomy selectively reduces the concentration of transforming growth factor beta in rat bone: implications for estrogen deficiency-associated bone loss.

Previous work showed that production of transforming growth factor beta (TGF-beta) by osteoblast-like rat UMR 106 cells was increased by 17 beta-estradiol at physiological concentrations. To determine whether ovariectomy alters the concentration of TGF-beta in rat long bones, female Sprague-Dawley rats were either sham-operated (n = 19) or ovariectomized (n = 19), pair-fed a semisynthetic diet for 6 weeks, and sacrificed. Tibial and femoral diaphyses were removed and extracted by demineralization. Ovariectomy lowered serum estrogen; did not alter body weight, serum magnesium, or serum 1,25-dihydroxyvitamin D; and produced only modest differences in serum calcium and phosphate concentrations. Hydroxyproline was higher and extractable protein was lower in bones from ovariectomized rats than in bones from sham-operated rats; calcium content did not differ between the two groups of animals. Ovariectomy lowered the concentration of TGF-beta in bone but did not change the concentration of insulin-like growth factors I or II compared with values in bone from control animals. The reduction of bone TGF-beta was evident 6 weeks after surgery but not at 3 weeks. Treatment of ovariectomized rats with estrogen eliminated the TGF-beta deficit. To determine whether 17 beta-estradiol increased TGF-beta production by normal bone cells, mouse osteoblasts were treated for 2 days with 17 beta-estradiol. The production of TGF-beta was increased almost 2-fold by 1 nM 17 beta-estradiol, and short-term treatment stimulated the intracellular accumulation of TGF-beta 1 mRNA. We conclude that ovariectomy reduces deposition of TGF-beta in rat bone and that diminished skeletal TGF-beta could play a role in the pathogenesis of bone loss, fractures, and microfractures that occur in estrogen-deficient states. Our results support the possibility that estrogen and bone TGF-beta may be necessary for normal maintenance of the skeleton in female rats.     

柚皮苷联合运动对去势大鼠骨量和骨强度的影响

目的观察柚皮苷（NG）联合中强度跑台运动对去势大鼠骨质疏松模型的治疗效果。方法2月龄雌性SD大鼠80只,用随机数字法分为假手术组（SHAM）、去势组（OVX）、去势＋不同浓度（40、100、200 mg/kg）柚皮苷组（OVX＋NG）、去势＋跑台＋柚皮苷组（OVX＋EX＋NG）、去势＋跑台组（OVX＋EX）、雌激素组（OVX＋E2）,每组10只。大鼠切除卵巢2个月后开始给药,给药60 d后观察各组大鼠股骨骨密度（BMD）,Micro-CT参数,血清生化指标及及股骨力学性能与组织学改变。结果柚皮苷与跑台运动干预60 d后,OVX＋EX＋NG组大鼠股骨颈力学强度、股骨BMD、BV/TV、Tb.N、Tb.Th等均高于单纯去势组（P〈0.05）,OVX＋EX＋NG组治疗效果与柚皮苷浓度呈正相关,以200 mg/kg柚皮苷效果最佳;200 mg/kg柚皮苷联合中强度跑台运动可进一步提高治疗效果。OVX＋NG组大鼠血清骨钙素升高,Ⅰ型胶原C端肽（CTX-1）降低;OVX＋EX组大鼠骨钙素与CTX-1均降低;OVX＋EX＋NG组大鼠骨钙素水平与柚皮苷组（200 mg/kg）无差异,但高于OVX＋EX。OVX＋EX＋NG组CTX-1水平低于单纯柚皮苷组和单纯跑台组（P〈0.05）。结论柚皮苷联合中强度跑台运动可提高去势大鼠股骨BMD,增加骨小梁数目,改善骨代谢指标,提高股骨力学性能。     

仙灵骨葆对去势大鼠骨量和生物力学性能的影响

目的探讨仙灵骨葆对骨质疏松(OP)大鼠骨量、骨代谢和生物力学性能的影响。方法 3月龄雌性SD大鼠24只分为3组,每组8只:正常对照组(N)、卵巢切除组(OVX)、卵巢切除+仙灵骨葆治疗组(XLGB)。除N组外,其余两组行卵巢切除术,6 w后XLGB组给予药物干预:250 mg.kg-1.d-1,OVX组给予等量生理盐水,8 w后处死所有大鼠。留取尿液、血清检测血PINP值、尿DPYD/Cr、NTX/Cr值。取左侧股骨行骨密度测定,取左侧胫骨制备硬组织不脱钙切片,备行骨组织形态计量学检测,取右侧股骨行三点弯曲试验,检测其最大载荷。结果 OVX组血PINP、尿DPYD/Cr、尿NTX/Cr值显著高于N组,XLGB能显著降低血PINP、尿DPYD/Cr、尿NTX/Cr值,但仍显著高于N组。OVX组股骨全长及近、中、远三段骨密度均显著低于N组,XLGB组近、远端骨密度显著高于OVX组。BV/TV在OVX组显著低于N组,XLGB组显著高于OVX组;OVX、XLGB组骨吸收指标Oc.N、Er.Pm均显著高于N组,XLGB组Oc.N、Er.Pm显著低于OVX组,BFR/BV显著高于OVX组。最大载荷三组之间无显著差别。结论仙灵骨葆灌胃可抑制卵巢切除大鼠骨量丢失,其机制与促进骨形成、抑制骨吸收,降低骨转换水平,进而维持骨量及微观结构有关。