骨骼肌卫星细胞移植对延缓失神经肌肉萎缩的作用

目的探讨骨骼肌卫星细胞移植对延缓失神经骨骼肌萎缩的作用,为提高治疗失神经骨骼肌萎缩的疗效提供依据。方法取成年SD大鼠32只,雌雄不限。随机分为2组,对照组与实验组各16只。两组均切断大鼠右后肢坐骨神经,并造成1cm神经缺损,形成失神经支配腓肠肌动物模型。无菌条件下切取SD大鼠双后肢及背部的肌肉,采用两步酶消化法分离肌卫星细胞,不连续密度梯度离心法纯化后体外培养,传代培养14～20d,细胞扩增至1×107/ml以上后准备移植。移植前1d以质量分数为0.02%的DAPI(4′-6-二脒基-2-苯吲哚)荧光标记肌卫星细胞过夜,实验组与对照组分别取肌卫星细胞悬液和生理盐水各0.2ml,注入腓肠肌内。术后第2、8周时取双侧腓肠肌测定肌湿重,然后行肌动蛋白免疫组织化学染色及HE染色,并作图像分析,测定肌纤维横截面积及肌动蛋白的含量,数据经SPSS10.0软件处理,行两组样本均数t检验。结果肌卫星细胞移植处可观察到带荧光的细胞核及肌纤维。实验组第2、8周时,失神经支配腓肠肌湿重残存率、腓肠肌纤维横截面积残存率、腓肠肌肌动蛋白含量与对照组相比差异有统计学意义(P<0.05)。结论肌卫星细胞移植到失神经骨骼肌内可明显延缓骨骼肌的萎缩。     

细胞外ATP防治失神经肌肉萎缩的实验研究

目的　探索细胞外ATP是否对失神经支配肌肉有保护作用。方法　SD大鼠 12只 ,在梨状肌下缘切断坐骨神经 ,制作腓肠肌失神经支配模型。左侧为实验组 ,术后于腓肠肌内注射ATP 0 .1mg/d ;右侧为对照组 ,腓肠肌内注射等量生理盐水。于术后 8、12周取 2组标本称肌湿重 ,检测运动终板、肌纤维横截面积及组织学变化。结果　实验侧的腓肠肌饱满有弹性、色泽好 ;对照侧肌纤维萎缩变细、色泽苍白。实验组运动终板边缘清晰 ,终板乙酰胆碱酯酶染色较深。比较两组的运动终板平均灰度值和平均光密度值 ,差异有显著性意义 (t =3 .0 5 7、4.13 8,P <0 .0 5 ) ,两组肌纤维横截面积相比 ,差异有显著性意义(t =4.191,P <0 .0 5 )。结论　ATP具有明显延缓失神经肌肉肌萎缩和减轻皮肤溃疡的作用     

选择性神经损伤对大鼠腓肠肌萎缩影响的实验研究

目的 研究单纯运动神经和／或感觉神经损伤对大鼠腓肠肌萎缩的影响。方法 本实验选用SD大鼠54只，分别切断左侧L4～L6脊神经前根、晤根或坐骨神经，建立大鼠选择性神经损伤模型。应用苏木精-伊红染色、AchE组织化学染色、透射电镜结合图象分析技术观察损伤岳2、4、10周大鼠腓肠肌湿重、肌细胞直径和截面积、运动终板面积和灰度及肌细胞趟微结构的变化，并作出综合评价。结果 损伤后2、4、10周，坐骨神经切断组大鼠腓肠肌的肌细胞直径及横截面积与前根切断组和聍根切断组相比较明显下降（P〈0．01）；坐骨神经切断组、前根切断组与后根切断组相比较，腓肠肌湿蓖显著下降（P〈0．05）；运动终板的横截面积明显减少、平均灰度显著增高（P〈0．01）。电镜观察发现，损伤后2周及4周，不同损伤模型大鼠腓肠肌肌细胞超微结构退变较轻、损伤后10周，肌丝、肌节排列紊乱甚至断裂、融合、缺失，肿胀或晕空泡状的线粒体逐渐增多，肌质网扩张，糖原颗粒明冠减少；不同损伤模型大鼠腓肠肌萎缩的形态学变化呈进行性加重，以坐骨神经切断组的变化最为明显，后根切断组的变化最轻。结论 运动神经及感觉神经对于骨骼肌的营养作用具有差蚌性，其巾运动神经对骨骼肌的营养起主要作用。     

壮骨强肌方对去势大鼠骨骼肌形态和功能的影响

目的 探讨壮骨强肌方对去卵巢模型大鼠的骨骼肌形态及功能的影响。方法 32只3月龄雌性SD大鼠常规饲养3个月后,随机分为假手术组8只和模型组24只,假手术组切除卵巢周围部分脂肪组织,模型组则切除双侧卵巢;术后喂养12周后,模型组再等分为3组,包括模型对照组、壮骨强肌方组和阿仑膦酸钠组,每组再抽取2只大鼠验证去卵巢模型造模成功。最后按照等效剂量换算公式予以各组灌胃处理,连续干预12周。灌胃结束后,测定大鼠的四肢抓力;取腓肠肌和比目鱼肌称重并计算骨骼肌质量指数,行HE染色观察肌纤维形态结构、测量肌纤维横截面积。结果 假手术组、壮骨强肌方组和阿仑膦酸钠组大鼠的四肢抓力、腓肠肌指数、小腿三头肌指数均明显高于模型组(P<0.05);假手术组和壮骨强肌方组的腓肠肌肌纤维平均横截面积均明显高于模型组(P<0.05),而阿仑膦酸钠组相对于模型组则无统计学意义(P>0.05);假手术组、壮骨强肌方组和阿仑膦酸钠组3者之间的差异均无统计学意义(P>0.05),在HE染色镜下3组大鼠的骨骼肌纤维形态结构均好于模型对照组。结论 壮骨强肌方能够明显改善去卵巢模型大鼠骨骼肌的形态和功能。     

血小板衍生生长因子-BB对去势大鼠退变关节的影响

我们通过去势大鼠动物模型，研究去势大鼠关节病理改变以及血小板衍生生长因子(PDGF)－BB对退变关节的生物学作用。材料与方法：取成年雌性SD大鼠54只，体重280～330g(平均305g)，随机分为正常组、去势组(OVX)组和治疗组，切除卵巢12周后，给予治疗组尾静脉注射。     

神经束植入联合甲钴胺治疗失神经骨骼肌的实验研究

目的研究神经束植入治疗失神经支配骨骼肌．并比较靶肌肉局部用药与全身性用药的疗效,探讨神经营养药物应用的最佳给药方法。方法选用雄性大鼠60只随机等分5组．每组12只,制作左侧胫神经切断动物模型。A组：神经束植入组;B纽：神经束植入＋左侧腓肠肌注射甲钴胺;C组：神经束植入＋腹腔注射甲钴胺;D组：胫神经切断：E组：胫神经切断＋左侧腓肠肌注射生理盐水。术后当日开始,B组隔日左侧腓肠肌注射甲钴胺300μg／kg;C组隔日腹腔注射甲钴胺300μg／kg;E组隔日左侧腓肠肌注射等渗盐水0．02ml。分别于术后4周和8周测量左小腿腓肠肌电生理、肌纤维横截面积和肌细胞TUNEL染色。结果术后4周及8周,A,B,C三组腓肠肌电位波幅组间比较差异均有显著性（P〈0．05）;D组与E组腓肠肌纤颤电位波幅差异无显著性（P〉0．05）。术后4周及术后8周,肌纤维横截面积和肌细胞TUNEL阳性细胞数A,B,C组间差异均有显著性（P〈0,05）,D,E组间差异无显著性（P〉0．05）,A,B,C组与D,E组差异有显著性（P〈0．05）。B组明显优于其他组。结论神经柬植入能有效防治失神经骨骼肌萎缩,靶肌肉给药效果优于全身用药。     

枸杞多糖对去势雌性大鼠骨质疏松的作用

目的研究枸杞多糖（LBP）对去势雌性大鼠骨质疏松的作用。方法选用2月龄成年雌性SD实验大鼠50只体重180~230g,随机分为5组,每组10只,选取1组大鼠打开腹腔切去少量腹腔脂肪组织,作为假手术组,其余4组大鼠切除双侧卵巢建立骨质疏松动物模型。各组给药干预,12周后行股骨干重测量、骨矿密度检查并观察骨的形态学改变。SPSS10.0统计软件分析查看各组是否有统计学意义。结果与去势＋生理盐水组相比,去势＋枸杞多糖高剂量组、去势＋枸杞多糖低剂量组均能增加去势雌性SD大鼠股骨干重、骨密度值,两组骨小梁结构较完整、连续性较好、吸收陷窝少。结论枸杞多糖对成年去势雌性大鼠骨质疏松有明显的治疗作用。     

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。     

RNA干扰介导的蛋白酶体亚基RC2下调延缓大鼠失神经骨骼肌萎缩

目的探讨RNA干扰（RNA interference, RNAi）介导的蛋白酶体亚基RC2（Rat component 2）下调延缓失神经肌萎缩的疗效。方法将48只SD大鼠，建立右下肢趾长伸肌失神经支配模型，随机分为实验组和对照组，每组24只。在电穿孔技术介导下，实验组和对照组分别转染含RC2基因和非同源对照序列的siRNA重组质粒溶液（0．8μg/μl）各50m。转染后3d，采用Western blot测定两组趾长伸肌中RC2蛋白含量；转染后14、21、28d，测定肌湿重维持率、肌肉蛋白含量和肌纤维横截面积，并观察肌纤维超微结构的变化。结果转染后3d，实验组RC2的蛋白水平明显下调，抑制率为25％，与对照组相比差异有统计学意义（P〈0．05）；转染后14d和21d实验组肌湿重维持率、肌肉蛋白含量和肌纤维横截面积均明显优于对照组（P〈0．05）；28d时，两组间各项指标差异无统计学意义（P〉0．05）。结论RNA干扰介导的蛋白酶体亚基RC2下调延缓失神经肌萎缩的疗效可以维持3周。     

鞘内复合应用氯胺酮和L-NAME对甲醛炎性疼痛大鼠脊髓c-fos表达的影响

目的观察鞘内复合应用非选择性一氧化氮合酶（NOS）抑制药-N^G-硝基-L-精氨酸-甲基酯（L-NAME）对氯胺酮抑制甲醛炎性疼痛大鼠脊髓后角c-fos表达效应的影响。方法选择鞘内置管后无神经损伤症状的雌性SD大鼠24只，随机均分为四组，分别经鞘内导管注入均为10μ1容量的生理盐水（K0组）、氯胺酮25μg（K1组）、氯胺酮150μg（K2组）和氯胺酮25μg加L-NAME100μg（KL组）。20min后在大鼠右足底皮下注射5％甲醛40μl，另选4只大鼠在右足底皮下注射生理盐水作为对照（N组）。观察大鼠的疼痛行为表现，并采用免疫组化方法检测脊髓后角FOS阳性细胞（FIL）的数目。结果K1、K2和KL组大鼠同侧脊髓后角FIL总数分别较K。组大鼠分别降低了32．4％、48．5％和39．1％。K1组和K：组大鼠脊髓后角板层Ⅰ～Ⅱ和板层Ⅴ～Ⅵ／Ⅹ内的FIL数目均显著低于K0组大鼠（P〈0．05），而KL组大鼠仅脊髓后角板层Ⅴ～Ⅵ／Ⅹ内的FIL数目显著低于K1组大鼠（P〈0．05）。结论鞘内注射氯胺酮呈剂量依赖性抑制甲醛炎性疼痛大鼠脊髓后角内c—fos的表达，并且复合应用L-NAME可选择性增强其对脊髓后角深层c—fos表达的抑制。     

雄激素对糖皮质激素致大鼠不同类型骨骼肌萎缩的拮抗作用研究

目的:探讨地塞米松对不同类型骨骼肌的致萎缩作用以及睾酮的拮抗效果.方法:雌性SD大鼠160只,随机分为4组(n=40):①对照组:前肢皮下注射芝麻油1 ml·kg-1·d-1,连续3 d后同时腹腔注射生理盐水1 ml·kg-1·d-1,每日1次;②地塞米松组:注射地塞米松1 mg·kg-1·d-1(代替生理盐水)和芝麻...     

血液透析患者微炎症状态与骨骼肌消耗性营养不良的临床研究

目的:明确血液透析患者循环炎症因子水平与营养状态及骨骼肌消耗的关系。方法:选择年龄和性别匹配的维持性血液透析患者62例,依据血清高敏C反应蛋白(high sensitivity C reactive protein,CRP)水平将患者分为两组:微炎症状组(CRP≥5 mg/L)、非微炎症状态组(CRP<5 mg/L)。主观全面营养评价法(SGA)评估患者营养状态,采集人体测量学数据,收集临床生化指标,Elisa方法检测CRP、白细胞介素-6(interleukin-6,IL-6)、肿瘤坏死因子-α(tumor necrosis factor alpha,TNF-α)等炎症因子水平,核磁共振(MRI)图像分析测量患者右下肢骨骼肌含量,分析肌肉横截面积(cross-sectional area,CSA)。结果:微炎症状态组的体重和体质量指数略低于非微炎症状态组,但SGA分值、人体测量学指标差异均无统计学意义;微炎症状态组的CRP和IL-6水平明显升高,但TNF-α在两组间差异无统计学意义;该组的血清白蛋白、前白蛋白、转铁蛋白水平显著降低,血红蛋白和红细胞比积略低于非炎症状态组,血脂、电解质等差异无统计学意义;MRI显示两组患者的肌肉组织均呈不同程度的萎缩,皮下脂肪分布不均匀,局部变薄,但微炎症状态组的肌肉萎缩更显著,肌肉横截面积(CSA)降低(P<0.05)。结论:持续性循环炎症因子水平升高所导致的机体微炎症状态,可引起血透患者营养指标降低,使血红蛋白更难达标,并加剧透析相关性骨骼肌消耗。微炎症状态可能是引起或加剧透析患者营养不良的重要原因。     

Low-intensity,high-frequency vibration appears to prevent the decrease in strength of the femur and tibia associated with ovariectomy of adult rats

The effect of low-intensity, high-frequency vibration on bone mass, bone strength, and skeletal muscle mass was studied in an adult ovariectomized (OVX) rat model. One-year-old female rats were allocated randomly to the following groups: start control, sham OVX, OVX without vibration, OVX with vibration at 17 Hz (0.5g), OVX with vibration at 30 Hz (1.5g), OVX with vibration at 45 Hz (3.0g). Vibrations were given 30 min/day for 90 days. During vibration each group of rats was placed in a box on top of the vibration motor. The amplitude of the vibration motor was 1.0 mm. The animals were labeled with calcein at day 63 and with tetracycline at day 84. The tibia middiaphysis was studied by mechanical testing and dynamic histomorphometry and the femur distal metaphysis by mechanical compression. OVX without vibration increased the periosteal bone formation rate and increased the medullary cross-sectional area, i.e., increased the endocortical resorption and outward anteromedial and lateral drifts of cortical bone at the tibia middiaphysis. OVX also resulted in a reduced maximum bending stress of the tibia diaphysis and a reduced compressive stress of the femur distal metaphysis. Vibration at the highest intensity, i.e., 45 Hz, of OVX rats induced a further increase in periosteal bone formation rate and inhibited the endocortical resorption seen in OVX rats. Furthermore, vibration at 45 Hz inhibited the decline in maximum bending stress and compressive stress induced by OVX. Neither OVX nor OVX with vibration influenced skeletal muscle mass. In conclusion, the results support the idea of a possible beneficial effect of passive physical loading on the preservation of bone in OVX animals.     

不同治疗时间脉冲电磁场对去势大鼠股骨骨密度的影响

目的 通过采用不同治疗时间脉冲电磁场(pulsed electromagnetic fields, PEMFs)干预去势大鼠骨质疏松模型,观察大鼠股骨骨密度变化,探索PEMFs治疗骨质疏松症的最佳治疗时间.方法 将50只雌性3月龄SD大鼠随机分为假手术组、卵巢切除(ovariectomy, OVX)对照组、OVX后不同时间治疗组(OVX Ⅰ组、OVX Ⅱ组及OVX Ⅲ组),每组10只.假手术组大鼠仅切除卵巢周围部分脂肪组织,不切除卵巢;余各组大鼠均切除双侧卵巢,制备去势大鼠骨质疏松模型.OVX Ⅰ组、OVX Ⅱ组和OVX Ⅲ组大鼠每天分别用强度3.8×10-10A/m、频率8Hz干预20、40及60min,共30d;假手术组和OVX对照组不干预.观察各组大鼠一般情况,并于干预结束后次日处死大鼠,作左侧股骨骨密度测定.结果 术后OVX对照组大鼠毛发逐渐稀疏,活动迟缓,精神萎靡不振,反应较为迟钝;其余4组大鼠毛发光洁,精神及活动正常.假手术组、OVX对照组、OVX Ⅰ组、OVX Ⅱ组及OVX Ⅲ组股骨骨密度分别为(0.226±0.011)、(0.210±0.011)、(0.231±0.013)、(0.231±0.017)及(0.229±0.013)g/cm2,OVX对照组骨密度低于其他组(P<0.05),假手术组、OVX Ⅰ组、OVX Ⅱ组及OVX Ⅲ组组间比较,差异无统计学意义(P>0.05).结论 每日采用PEMFs对去势大鼠治疗20～60min能阻止其骨密度下降,接近正常水平,对骨质疏松症有良好的预防作用,且3种治疗时间对骨密度的维持效果相同.     

Reinnervation of denervated muscle in a split-nerve transfer model

This study was performed to quantify the reinnervation of denervated muscle in a split-nerve transfer model and to determine any possible downgrading effects on the donor nerve and its end organ. Fifty-four adult Wistar rats weighing 200 to 250 g were used. The experimental design consisted of two groups. The motor nerve branch to the anterior tibial muscle and gastrocnemius muscle of the right hind limb were dissected in all rats. In the experimental group (N = 36), the motor nerve branch of the tibial nerve to the gastrocnemius muscle was exposed, cut, and ligated. The motor nerve branch to the anterior tibial muscle was split and transected longitudinally, and the medial half was routed posteriorly. End-to-end neural anastomosis was performed between this medial half of the split nerve and the distal stump of the gastrocnemius nerve. In the control group (N = 18), while the same surgical preparation was performed, the motor nerve branch to the anterior tibial muscle and gastrocnemius nerve were exposed and transected, and the nerve endings were ligated, but neural anastomosis was not performed between these nerves. The left hind limb of all rats served as a normal comparison side without any surgical intervention. Both of the groups were divided into three subgroups (12 rats each for the experimental groups and 6 rats each for the control group) to evaluate the results after periods of 1, 3, and 6 months. Electromyography, light microscopic and morphometric examination, and muscle weight measurements were used to document the results. Although stimulation of the peroneal and tibial nerves did not produce any compound muscle action potential (CMAP) recordings from either the anterior tibial or the gastrocnemius muscle in the control group, the normalized CMAP areas of the tibial nerve were (mean +/- standard deviation) 16.2 +/- 30.8% in the 1-month group, 63.4 +/- 34.7% in the 3-month group, and 72.4 +/- 16.3% in the 6-month group. For the peroneal nerve, the normalized CMAP areas were 17.0 +/- 32.2%, 53.4 +/- 29.4%, and 54.4 +/- 14.5% for the 1-, 3-, and 6-month groups in the experimental groups respectively. A high number of regenerating myelinated nerve fibers was identified in the distal part of the coapted motor nerve branch to the gastrocnemius muscle. The average number of myelinated fibers in the lateral half of the split nerve in the experimental group was 15,108 fibers per square millimeter, 14,167 fibers per square millimeter, and 19,830 fibers per square millimeter at months 1, 3, and 6 respectively. The average number of fibers proximal to the nerve anastomotic site was 15,423 fibers per square millimeter, 19,200 fibers per square millimeter, and 20,774 fibers per square millimeter. Distal to the nerve anastomotic site, the number of myelinated fibers was 17,941 fibers per square millimeter, 18,885 fibers per square millimeter, and 18,895 fibers per square millimeter at 1, 3, and 6 months respectively. There were no myelinated fibers in the control group sections. There were significant differences in muscle weight between the experimental and control groups at the end of month 6. The difference between the experimental side and the untouched normal healthy side was not significant in the weight measurements of both muscles. The results show acceptable reinnervation by split-nerve transfer with minimal functional impairment of the donor muscle. This study confirms that split-nerve transfer is a reliable method of reconstruction for paralyzed muscle with minimal donor area morbidity.     

大鼠肢体急性和慢性缺血病变特点的对照研究

目的 建立大鼠急性和慢性后肢缺血模型,研究两组大鼠病变特点及缺血代偿情况.方法 选择3 月龄成年、高脂血症SD 大鼠建立急性（n = 20）和慢性（n = 20）后肢缺血模型.采用实时荧光定量PCR 和2-△△Ct 法,检测股动脉闭塞后6 h 患肢股内收肌血管内皮生长因子（VEGF）和缺氧诱导因子（HIF-1α）的相对定量.股动脉闭塞1 周后取腓肠肌检查组织坏死及炎症浸润情况.股动脉闭塞后4 周后采用免疫组织化学染色法计算股内收肌毛细血管/肌纤维比例.术后记录患肢运动功能及患肢/健肢股骨中段周径比值.结果 急性组大鼠术后即刻表现严重肢体缺血.慢性组平均术后（8.2 ± 0.7）d 始表现严重肢体缺血.股动脉闭塞后6 h,急性组股内收肌目标基因VEGF和HIF-1α的相对定量均高于慢性缺血组[（5.57 ± 0.87） vs.（2.49 ± 0.85）和（10.28 ± 1.09） vs.（6.83 ±1.17）,P 〈 0.05].股动脉闭塞后1 周,急性组腓肠肌病理组织学检查显示较多坏死及炎症浸润.股动脉闭塞后4 周,急性组股内收肌毛细血管/肌纤维比例显著高于慢性组[（1.37 ± 0.14） vs.（1.18 ±0.12）,P 〈 0.05].缺血肢体功能评分结果 显示,急性缺血肢体运动功能早期受损甚于慢性组（P 〈0.05）,但后期恢复较优（P 均〈 0.05）.结论 急、慢性缺血具有不同的病理损伤特点,进而表现出不同的缺血代偿机制.急性大鼠缺血的代偿优于慢性缺血.     

Low-magnitude whole body vibration does not affect bone mass but does affect weight in ovariectomized rats

Mechanical loading has stimulating effects on bone architecture, which can potentially be used as a therapy for osteoporosis. We investigated the skeletal changes in the tibia of ovariectomized rats during treatment with whole body vibration (WBV). Different low-magnitude WBV treatment protocols were tested in a pilot experiment using ovariectomized rats with loading schemes of 2 × 8 min/day, 5 days/week (n = 2 rats per protocol). Bone volume and architecture were evaluated during a 10 week follow-up using in-vivo microcomputed tomography scanning. The loading protocol in which a 45 Hz sine wave was applied at 2 Hz with an acceleration of 0.5g showed an anabolic effect on bone and was therefore further analyzed in two groups of animals (n = 6 each group) with WBV starting directly after or 3 weeks after ovariectomy and compared to a control (non-WBV) group at 0, 3, 6 and 10 weeks’ follow-up. In the follow-up experiment the WBV stimulus did not significantly affect trabecular volume fraction or cortical bone volume in any of the treatment groups during the 10 week follow-up. WBV did reduce weight gain that was induced as a consequence of ovariectomy. We could not demonstrate any significant effects of WBV on bone loss as a consequence of ovariectomy in rats; however, the weight gain that normally results after ovariectomy was partly prevented. Treatment with WBV was not able to prevent bone loss during induced osteoporosis.     

大鼠失神经支配骨骼肌萎缩后肌细胞凋亡及Bcl-2、Bax表达的变化

目的 研究失神经支配骨骼肌萎缩后肌细胞凋亡及Bcl-2、Bax表达的变化规律.方法 实验以失神经支配腓肠肌为动物模型.选用体质量为200～250 g的雌性SD大鼠42只,随机分成2组,实验组36只,健康对照组6只.按术后取材时间的不同再将实验组分为6组,每组6只大鼠.分别运用Tunel法及免疫组织化学方法检测失神经后不同时间萎缩腓肠肌细胞凋亡及Bcl-2、Bax的表达变化,同时测量肌湿重比和肌纤维横截面积,透射电镜观察肌细胞的超微结构变化.结果 萎缩的腓肠肌湿重比在失神经4周内和第10周到第12周下降最快,而在第4周到10周和第12周到16周下降较慢,且变化差异无统计学意义(P＞0.05).Bcl-2仅在失神经早期表达增高,于第4周达高峰;而Bax分别于失神经第2周与第12周达高峰,增高幅度大于Bcl-2.Bcl-2/Bax的比值除对照组(1.522±0.215)和失神经第8周时(1.065±0.165)大于1外,其余各时间点均小于1.肌细胞凋亡率分别于失神经第4周和第12周达到高峰,其变化趋势与Bax相仿.结论 失神经腓肠肌萎缩过程呈现4个阶段;凋亡和凋亡相关基因Bax过量表达在失神经不可逆肌萎缩过程中发挥着重要的作用;靶向作用Bax基因,抑制Bax表达可能延缓失神经骨骼肌萎缩.     

不同浓度乙醇对大鼠肌肉组织影响的探讨

目的：探讨不同浓度乙醇对大鼠腓肠肌功能及组织学的影响。方法：选取等重的雄性SD大鼠75只,随机分入A、B、C、D、E五组,在各组大鼠左侧腓肠肌注射0.2ml浓度分别为50%、60%、70%、80%、90%的乙醇,右侧均注射相同量的生理盐水。分别于注射后第3、7、14、21和28天分离大鼠左右侧腓肠肌,检测每只大鼠左右侧腓肠肌的收缩力差（ΔF）及肌体积差（ΔV）,并取标本做HE染色,光镜下观察肌肉组织学变化。结果：注射相同天数,实验组A、B、C、D组ΔF与ΔV随乙醇浓度增加而明显升高（P〈0.05）,D组与E组之间无显著差异（P〉0.05）;同一乙醇浓度下,三周内,ΔF与ΔV均随时间延长而明显增加（P〈0.05）,与注射后第21天相比,注射后28天无明显差异（P〉0.05）。光镜下,随着时间延长及浓度增大腓肠肌纤维化程度明显加重。结论：随着浓度（50%～80%）增加,乙醇对大鼠腓肠肌损伤程度加重;当乙醇浓度超过80%时,腓肠肌收缩功能基本丧失及组织学上基本纤维化。注射21天后,肌肉组织纤维化程度基本稳定。