活性氧、线粒体通透性转化孔介导肌细胞凋亡在失神经骨骼肌萎缩中的相关性

目的 观察活性氧(ROS)、线粒体通透性转化孔(MPTP)在失神经骨骼肌萎缩后的表达变化且与肌细胞凋亡的相关性,探讨ROS、MPTP参与失神经骨骼肌萎缩的具体分子机制.方法 将30只Vistar大鼠随机分为对照组、失神经2d组、失神经7d组、失神经14d组、失神经28d组,每组6只.制作坐骨神经切断后失神经支配的腓肠肌Vistar大鼠模型.应用流式细胞术(FCM)检测失神经支配后腓肠肌细胞ROS的含量,激光共聚焦显微镜检测MPTP的开放,脱氧核糖核苷酸转移酶介导的缺口末端标记(TUNEL)法检测肌细胞凋亡.结果 大鼠失神经支配后,肌细胞中的ROS、MPTP及凋亡率与正常对照组比较,表达随失神经支配时间的延长(<28d)而持续增加,且各组的表达均显著高于对照组(P<0.05),ROS的表达与MPTP的开放呈正相关(r=0.884,P<0.01),与肌细胞的凋亡率呈正相关(r=0.893,P<0.01),MPTP的开放与肌细胞凋亡率呈正相关(r=0.927,P<0.01)与肌细胞萎缩指标肌湿重比呈负相关(r=-0.907,P<0.01).结论 ROS、MPTP为调控失神经支配后骨骼肌萎缩的重要分子,其具体机制是通过线粒体介导的凋亡通路促进骨骼肌萎缩.

Abstract：

Objective To study the expression of reactive oxygen species (ROS) and mitochondrial permeability transition pore (MPTP) in denervated skeletal muscle atrophy and its correlation with cell apoptosis, and explore specific molecular mechanism in denervated skeletal muscle atrophy. MethodsThirty Vista rats were randomly divided into five group: control group, 2-days group, 7-days group, 14-days group, 28-days group. Standard model of denervated gastrocnemius muscle was established. The content of ROS and the opening of MPTP in the gastrocnemius were detected by flow cytometry (FCM) and fluorescence microscope respectively. The apoptotic cells in atrophic muscle were examined by TdT-mediated dUTP nick end labeling (TUNEL). Results As compared with the control group, the content of ROS, the opening of MPTP and the apoptosis of gastrocnemius were increased continuously (<28 days) in 2-days group, 7-days group, 14-days group, 28-days group (P<0.05). The content of ROS had a positive correlation with the opening of MPTP (r=0.884,P<0.01) and the apoptosis rate (r=0.893,P<0.01), and the opening of MPTP had a positive correlation with the apoptosis rate (r=0.927,P<0.01), but a negtive correlation with the ratio of muscle wet weight (r=-0.907,P<0.01). Conclusion ROS and MPTP are important elements in regulating skeletal muscle atrophy after denervation by the mitochondrial apoptosis pathway.     

失神经骨骼肌NF-kappa B的表达变化与线粒体通透性转换孔开放及细胞凋亡的关系

目的 通过研究去神经骨骼肌细胞核转录因子kappa B(nuclear factor of kappa B,NF-kappa B)p65与线粒体通透性转换孔(mitochondrion permeability transition pore,MPTP)及细胞凋亡的关系,探讨失神经肌萎缩的相关机制.方法 Wistar大鼠30只,随机分为健康对照组、去神经2 d组、去神经7 d组、去神经14 d组、去神经28 d组.建立右下肢腓肠肌失神经支配模型,对照组仅做假手术.采用Western Bloting检测大鼠腓肠肌NF-kappa B p65蛋白表达水平,共聚焦荧光显微镜观察MPTP的开放情况,脱氧核糖核苷酸转移酶介导的缺口末端标记(Tunnel)技术检测细胞凋亡情况,并结合肌湿重进行相关性分析.结果 大鼠失神经支配后随着肌湿重比的下降,NF-kappa B p65蛋白、MPTP的开放以及骨骼肌细胞的凋亡率在各个时间点持续增加,且明显高于对照组,差异有统计学意义(P＜0.05),NF-kappa B与MPTP的开放(r=-0.896,P＜0.01)以及凋亡率(r=0.890,P＜0.01)密切相关,并且NF-kappa B和凋亡率的升高与肌湿重比呈负相关关系(r分别为-0.919、-0.924,P均＜0.01).结论 NF-kappa B在失神经肌萎缩中起重要作用,其作用机制与MPTP的开放及细胞凋亡有关.

Abstract：

Objective To analyze the relationship of nuclear factor of kappaB (NF-κB) p65 to mitochondrion permeability transition pore (MPTP) and apoptosis during denervation atrophy of the gastrocnemius muscle, and delineate their potential roles in skeletal muscle atrophy. Methods Thirty Wistar rats were randomly divided into 5 groups: control group, 2 day denervation group, 7 day denervation group, 14 day denervation group, and 28 day denervation group. The gastrocnemius muscle was denervated by transection of the sciatic nerve. Sham operation was done in the control group. Levels of NF-κB p65 protein and the opening of the mitochondrial permeability transition pore in the gastrocnemius muscle were detected respectively by Westem Bloting and confocal fluorescence microscopy. The apoptotic cells in atrophic muscles were quantitated with Tunel. Muscle wet weight was also measure for comparison. Results At different time points after denervation, the levels of NF-κB p65, the opening of MPTP and apoptosis of gastrocnemius were significantly higher than those in the normal group ( P ＜ 0.05). Furthermore NF-κB p65 had a positive correlation with the opening of MPTP (r= - 0.896, P ＜ 0.01) and with the ratio of apoptosis (r = 0.890,P ＜0.01 ), while the increase of NF-κB p65 and apoptosis was negatively correlated with the ratio of muscle wet weight ( r = - 0. 919,-0.924, P ＜ 0.01 ). Conclusion NF-κ3 plays an important role in denervation skeletal muscle atrophy.This effect is related to the opening of MPTP and apoptosis.     

慢性压迫性脊髓损伤后大鼠运动功能及周围神经和骨骼肌中胰岛素样生长因子-1表达的变化

目的 观察慢性压迫性脊髓损伤后大鼠运动功能变化及周围神经和骨骼肌中胰岛素样生长因子-1(IGF-1)表达变化.方法 将50只Wistar雌性大鼠随机分为正常组、假手术组和慢性压迫组.慢性压迫组置入平头塑料螺钉对大鼠脊髓进行后路渐进性压迫,于2个月后分别压迫至20%、40%、60%左右程度.行神经功能观察;处死大鼠后取腓肠肌作为标本,分别进行IGF-1的免疫组织化学和原位杂交染色.结果 大鼠后肢瘫痪程度随压迫程度加重而加重,各组坐骨神经和骨骼肌中IGF-1蛋白和mRNA表达分别为:20%组(236.9±3.2)、(231.5±2.9)、(245.6±3.4)、(246.6±2.7);40%组(205.3±2.7)、(202.2±3.4)、(209.4±2.6)、(214.6±2.5);60%组(215.4±3.5)、(219.3±4.1)、(231.9±2.3)、(238.5±2.7).各压迫组坐骨神经及骨骼肌中IGF-1 mRNA和蛋白表达增加,与正常组比较差异有统计学意义(P<0.05).结论脊髓压迫性损伤可引起周围神经及骨骼肌中IGF-1表达增加,提示机体调动保护因素以减轻脊髓损伤并促进其再生.

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Objective To observe the changes in motor function and expression of insulin-like growth factor-1 (IGF-1) of peripheral nerve and skeletal muscle in rats after chronic spinal cord compression. Methods A total of 50 Wistar rats were randomly divided into normal group (n=10), sham operation group (group A,n=10) and chronic compressive group (goup B,n=30). The rats in group B were given gradual compression on the posterior spinal cord using blunt plastics screw. Compression degree reached 20% (n=10), 40% (n=10) and 60% (n=10) respectively after two months. The rats were killed, and gastrocnemius muscle cells were removed. The expression levels of IGF-1 protein and mRNA in peripheral nerve and skeletal muscle were detected by immunohistochemistry and hybridization respectively after chronic compressive spinal cord injury. Results The rat hind limb paralysis was exacerbated with the increase of the compression. In the sciatic nerve and skeletal muscle, the expression levels of IGF-1 protein and mRNA were: (236.9±3.2), (231.5±2.9), (245.6±3.4), (246.6±2.7) in 20% group; (205.3±2.7), (202.2±3.4), (209.4±2.6), (214.6±2.5) in 40% group; (215.4±3.5), (219.3±4.1), (231.9±2.3), (238.5±2.7) in 60% group. The expression levels of IGF-1 protein and mRNA in peripheral nerve and skeletal muscle were significantly up-regulated after compression (P<0.05). Conclusion The results indicate that body transfers the protective factor to relieve injury of CNS.     

周围神经损伤修复后早期骨骼肌细胞凋亡的初步研究

Objective To explore skeletal muscle apoptosis at the early stage of peripheral never regeneration in rats.Methods A total of 54 male SD rats were randomly assigned to 3 groups ( n = 18/group): denervation group (A), neurorrhaphy group (B), normal control group (C).In group A, a 1 cm segment of the left sciatic nerve was removed.In group B, the left sciatic nerve was transected above the bifurcation and immediately repaired with 10-0 sutures.No surgery was done in group C.The gastrocnemius muscle wet weight served as an indicator of the degree of muscle atrophy.Marker of apoptosis, nuclear DNA fragmentation, was detected using terminal deoxyribnudeotidyl transferase mediated dUTP nick end labeling (the TUNEL method) and observed under confocal microscopy at 2, 14 and 28 days postoperatively.Another portion of the gastrocnemius muscle was homogenized to analyze the activity of caspase-3 and -8 by spectrophotometry.Results TUNEL labeling of fragmented DNA on histological sections in the neuorrhaphy group revealed levels of apoptotic nuclei higher than the control group and lower than the denervation group at the early stage ( ＜ 28days ).The activity of caspase-3 and -8 in the neuorrhaphy group was also higher than the control group but lower than the denervation group.Conclusion At the initial stage of peripheral never regeneration, apoptosis may contribute to muscle atrophy and extrinsic apoptotic pathways may take part in it.     

周围神经损伤修复后早期骨骼肌细胞凋亡的初步研究

Objective To explore skeletal muscle apoptosis at the early stage of peripheral never regeneration in rats.Methods A total of 54 male SD rats were randomly assigned to 3 groups ( n = 18/group): denervation group (A), neurorrhaphy group (B), normal control group (C).In group A, a 1 cm segment of the left sciatic nerve was removed.In group B, the left sciatic nerve was transected above the bifurcation and immediately repaired with 10-0 sutures.No surgery was done in group C.The gastrocnemius muscle wet weight served as an indicator of the degree of muscle atrophy.Marker of apoptosis, nuclear DNA fragmentation, was detected using terminal deoxyribnudeotidyl transferase mediated dUTP nick end labeling (the TUNEL method) and observed under confocal microscopy at 2, 14 and 28 days postoperatively.Another portion of the gastrocnemius muscle was homogenized to analyze the activity of caspase-3 and -8 by spectrophotometry.Results TUNEL labeling of fragmented DNA on histological sections in the neuorrhaphy group revealed levels of apoptotic nuclei higher than the control group and lower than the denervation group at the early stage ( ＜ 28days ).The activity of caspase-3 and -8 in the neuorrhaphy group was also higher than the control group but lower than the denervation group.Conclusion At the initial stage of peripheral never regeneration, apoptosis may contribute to muscle atrophy and extrinsic apoptotic pathways may take part in it.     

周围神经损伤修复后早期骨骼肌细胞凋亡的初步研究

目的 探讨神经修复后早期大鼠骨骼肌的细胞凋亡情况.方法 取SD大鼠54只,随机分为3组:失神经组(A组)18只,神经缝合组(B组)18只,健康对照组(C组)18只.A组大鼠切除左侧1 cm长坐骨神经,B组大鼠横断左侧坐骨神经后立即用10-0医用尼龙线行外膜缝合,C组大鼠不做任何处理.以腓肠肌肌湿重作为骨骼肌萎缩指标.分别应用脱氧核糖核苷酸末端转移酶介导的缺口末端标记法(TUNEL)和分光光度法检测术后2 d、14 d、28 d时骨骼肌凋亡细胞核和天冬氨酸特异性半胱氨酸蛋白酶(Caspase)-3与Caspase8活性.结果 神经缝合后早期骨骼肌与正常骨骼肌比较,细胞凋亡现象增加,凋亡相关蛋白Caspase-3和Caspase-8活性上升,但程度弱于失神经骨骼肌.结论 细胞凋亡可能是神经修复后早期骨骼肌萎缩原因之一,死亡受体信号通路参与神经修复后早期骨骼肌凋亡过程中.

Abstract：

Objective To explore skeletal muscle apoptosis at the early stage of peripheral never regeneration in rats.Methods A total of 54 male SD rats were randomly assigned to 3 groups ( n = 18/group): denervation group (A), neurorrhaphy group (B), normal control group (C).In group A, a 1 cm segment of the left sciatic nerve was removed.In group B, the left sciatic nerve was transected above the bifurcation and immediately repaired with 10-0 sutures.No surgery was done in group C.The gastrocnemius muscle wet weight served as an indicator of the degree of muscle atrophy.Marker of apoptosis, nuclear DNA fragmentation, was detected using terminal deoxyribnudeotidyl transferase mediated dUTP nick end labeling (the TUNEL method) and observed under confocal microscopy at 2, 14 and 28 days postoperatively.Another portion of the gastrocnemius muscle was homogenized to analyze the activity of caspase-3 and -8 by spectrophotometry.Results TUNEL labeling of fragmented DNA on histological sections in the neuorrhaphy group revealed levels of apoptotic nuclei higher than the control group and lower than the denervation group at the early stage ( ＜ 28days ).The activity of caspase-3 and -8 in the neuorrhaphy group was also higher than the control group but lower than the denervation group.Conclusion At the initial stage of peripheral never regeneration, apoptosis may contribute to muscle atrophy and extrinsic apoptotic pathways may take part in it.     

缺血后处理对大鼠肝缺血再灌注时肝细胞线粒体膜通透性转换和膜电位的影响

目的 评价缺血后处理对大鼠肝缺血再灌注时肝细胞线粒体膜通透性转换和膜电位(△Ψm)的影响.方法 成年健康雄性SD大鼠40只,体重220～260 g,采用随机数字表法,将其随机分为5组(n=8):假手术组(S组)、苍术苷+假手术组(A+S组)、缺血再灌注组(IR组)、缺血后处理组(IPO组)和苍术苷+缺血后处理组(A+IPO组).采用阻断肝中叶和左叶60 min,恢复血流灌注6 h的方法 建立大鼠肝缺血再灌注模型.S组和A+S组仅游离肝门,不阻断血管;A+S组关腹前静脉注射苍术苷5 mg/kg;IR组制备肝缺血再灌注模型;IPO组于再灌注前行缺血后处理,再灌注1 min,缺血1 min,反复3次;A+IPO组于再灌注前静脉注射苍术苷5 mg/kg.于缺血前即刻和再灌注6 h时,采集左颈静脉血样,测定血清ALT和AST的活性.再灌注6 h时处死大鼠,取肝左叶组织,观察超微结构和细胞凋亡情况,计算凋亡指数,测定细胞色素c(Cyt c)的表达水平、△Ψm和线粒体通透性转换孔(MPTP)活性.结果 与S组比较,A+S组时血清ALT和AST的活性、凋亡指数、Cyt c表达、△Ψm和MPTP活性差异无统计学意义(P＞0.05),IR组、IPO组和A+IPO组再灌注6 h时血清ALT和AST的活性、凋亡指数升高,Cyt c表达上调,△Ψm降低,MPTP活性升高(P＜0.05);与IR组比较,IPO组血清ALT和AST的活性、凋亡指数降低,Cyt c表达下调,△Ψm升高,MPTP活性降低(P＜0.05),肝组织病理学损伤减轻,A+IPO组各指标差异无统计学意义(P＞0.05);与IPO组比较,A+IPO组血清ALT和AST的活性、凋亡指数升高,Cyt c表达上调,△Ψm降低,MPTP活性升高(P＜0.05),肝组织病理学损伤加重.结论 缺血后处理可抑制肝细胞线粒体膜通透性转换,减少线粒体△Ψm的耗散,从而减轻大鼠肝缺血再灌注损伤.

Abstract：

Objective To investigate the effects of ischemic postconditioning on mitochondrial permeability transition and mitochondrial transmembrane potential(△Ψm)following hepatic ischemia-reperfusion(I/R)in rats.Methods Forty male SD rats weighing 220-260 g were randomly divided into 5 groups with 8 animals in each group:sham operation group(group S);atractyloside+sham operation group(group A+S);I/R group;ischemic postconditioning group(group IPO)and atractyloside+ischemic postconditioning group(group A+IPO).The animals were anesthetized with intramuscular injection of atropine 0.05 mg/kg.Hepatic I/R was produced by occlusion of hepatic blood flow for 60 min followed by 6 h reperfusion.In group A+S,atractyloside 5 mg/kg was injected intravenously before abdomen Was closed.In group IPO,the animals were subjected to 3 cycles of 1 min reperfusion interspersed with 1 min hepatic isehemia at the end of 60 min hepatic ischemia.In group A+IPO,atractyloside 5 mg/kg was injected intravenously before reperfusion. Venous blood samples were collected for determination of serum ALT and AST activities immediately before ischemia and at 6 h of reperfusion. The animals were then sacrificed.Their livers were removed for microscopic examination, detection of apoptosis and determination of cytochrome c (Cyt c) expression, △Ψm and mitochonerial permeability transition pore (MPTP)activity. Apoptosis index (AI) was calculated. Results There was no significant difference in serum ALT and AST activities, AI, Cyt c expression, △Ψm and MPTP activity between S and A + S groups (P＞0.05). Compared with group S, serum ALT and AST activities and AI were significantly increased, Cyt c expression was up-regulated, △Ψm was decreased and MPTP activity was increased in groups I/R, IPO and A+IPO(P＜0.05).Compared with group I/R, serum ALT and AST activities and AI were significantly decreased,Cyt c expression was down-regulated, △Ψm was increased and MPTP activity was decreased in group IPO(P＜0.05), while no significant change was found in group A+IPO(P＞0.05).Compared with group IPO,serum ALT and AST activities and AI were significantly increased, Cyt c expression was up-regulated, △Ψm was decreased and MPTP activity was increased in group A + IPO(P＜ 0.05).Microscopic examination showed that hepatic injury was reduced in group IPO compared with group I/R, while aggravated in group A+ IPO compared with group IPO. Conclusion Ischemic postconditioning can protect liver from I/R injury by attenuating the I/R-induced increase in MPTP opening and decrease in △Ψm in rats.     

慢性肾衰竭大鼠肠道通透性及损伤的研究

Objective To observe the histopathologic injury of small intestine and intestinal permeability in chronic renal failure (CRF) rats. Methods Twenty male Sprague-Dawley rats were randomly assigned to CRF group (n=10) and control group (n=10). 5/6 nephrectomy was used to establish CRF rats, while sham operation for control. Blood biochemistry was regularly monitored until CRF model was successfully established. The model rats were fed with lactulose (L) and mannitol (M) through intragastric administration. Urine was collected after 6 hours, and the concentration of lactulose and mannitol in urine was measured using high pressure liquid chromatograph with refractive index detector (HPLC-RID), and the ratio of urinary excretion of L/M was calculated to evaluate intestinal permeability. Small intestinal mucosa were stained by hematoxylin-eosin (HE) and observed with light microscope (villus height, thickness of muscle layer and villus count), histological damage score was used to evaluate intestinal injury. Results The L/M ratio of CRF group was higher than that of control group (1.75±0.11 vs 1.20±0.06, P<0.01). The small intestinal mucosal villus height and thickness of muscle layer in CRF group were higher (P<0.01), and the number of villi was lower compared to control group (P<0.01). The score of histopathologic intestine damage of CRF group was higher than that of control group (1.00±0.71 vs 0, P<0.01). Conclusion The intestinal permeability of CRF rats is increased with varying degrees of intestinal damage.     

绝经后妇女身高缩短程度与骨质疏松发生的关系研究

目的探讨绝经后妇女身高缩短程度与骨质疏松发生的关系。方法随机选择绝经后妇女进行健康问卷调查,包括现在、年轻时身高;用双能X线骨密度仪测定腰椎、髋部骨密度,分为骨质疏松组和无骨质疏松组;用SPSS 20.0统计软件统计分析。结果共筛选入组263例,骨质疏松组160例、无骨质疏松组103名:(1)两组资料的一般比较:年龄、身高缩短(H/cm)、BMI、膝关节炎、腰椎间盘突出等因素差异具有统计学意义(P0.05),身高、体重、绝经年龄等因素无统计学意义(P0.05);(2)各因素与骨密度的相关性分析:身高缩短、关节炎等因素与腰椎、髋部骨密度呈负相关,腰椎间盘突出与腰椎骨密度呈负相关、与髋部骨密度无相关性;以身高缩短作为因变量,骨质疏松、关节炎、腰椎间盘突出为变量进行多重线性回归分析:y=0.027+0.008×骨质疏松+0.009×膝关节炎+0.003×腰椎间盘突出,标准回归系数依次为0.183、0.171、0.063,骨质疏松对身高缩短程度影响最大,其次是膝关节炎;(3)263例不同身高缩短的分布情况:身高缩短H3 cm,无骨质疏松和有骨质疏松占各本组的31.1%和50.0%;从箱式图可以知道三组身高缩短均值从高到低依次是:重度骨质疏松、轻度骨质疏松、无骨质疏松。结论绝经后妇女身高缩短与骨密度呈负相关,骨质疏松能够影响身高缩短,身高缩短越大骨质疏松越严重。身高缩短3 cm时提示可能发生骨质疏松。     

老年男性骨质疏松症与血清痩素水平关系的研究

目的 探讨瘦素和老年男性骨质疏松的关系.方法 选择86例老年男性原发骨质疏松患者和50例正常对照者,采用放免法检测血清瘦素(Lep)浓度,骨钙素(BGP)、I型胶原前胶原氨基端前肽(PINP),采用双能X线吸收法测定腰椎及髋部骨密度,同时计算体重指数(body mass index, BMI),并分析瘦素与其他各项指标的关系.结果 老年男性骨质疏松组血清瘦素水平(4.137±2.439 μg/L)明显低于正常对照组(5.142±2.869 μg/L),两组有显著性差异,P<0.05.血清瘦素水平与BMI显著正相关(Pearsons 相关系数r=0.470, P<0.001),亦与L_(1-2), L_4的BMD 及BGP正相关(r分别为0.356,0.315,0.307,0.241, P<0.05),但在校正BMI后,瘦素与L_2的BMD及BGP的正相关关系消失,与L_1(r=0.193,P<0.05)和L_4(r=0.212, P<0.05)BMD的正相关关系亦有所减弱.结论 老年男性骨质疏松患者血清瘦素水平下降,推测瘦素可能通过外周局部作用影响骨代谢.     

铁死亡血清学标志物在绝经后骨质疏松症发病中的作用及预测模型构建

目的 探索铁死亡血清生物标志物谷胱甘肽过氧化酶4(GPX4)、谷胱甘肽(GSH)以及丙二醛(MDA)和绝经后骨质疏松症(postmenopausal osteoporosis, PMOP)发病的关系及对其的预测价值。方法 以80名绝经后女性作为研究对象，按照骨质疏松症诊断标准分为骨质疏松组(60例)和非骨质疏松组(20例)。比较两组受试者一般资料及血清GPX4、GSH、MDA水平；Spearman相关分析各变量和骨密度及各变量之间的相关性；随机森林算法评估各变量对PMOP发病的重要性；ROC曲线进一步肯定各变量对PMOP的预测效能。最后，构建PMOP预测模型。结果 两组受试者体质量指数、体重、身高相比无明显差异(P>0.05);非骨质疏松受试者腰椎骨密度、GPX4、GSH水平均比骨质疏松症组高，年龄、MDA值则比骨质疏松组低(P<0.05)。Spearman相关分析显示，随着GPX4水平(R=0.42,P<0.05)、GSH水平(R=0.43,P<0.05)升高，受试者骨质疏松程度越低；随着MDA水平(R=-0.30,P<0.05)升高，受试者骨质疏松程度...     

绝经后骨质疏松症中医证型与握力的研究

目的 探讨绝经后骨质疏松症(postmenopausal osteoporosis,PMOP)患者中医证型与握力的关系.方法 选取2017年11月至2018年10月在济南各社区及山东中医药大学附属医院骨质疏松门诊纳入的绝经后骨质疏松症女性142例(骨质疏松组)、绝经后非骨质疏松症女性39例(非骨质疏松组).依照中医辨证...     

强直性脊柱炎患者血清TNF-a、BGP和CTX水平与骨密度的关系

目的探讨强直性脊柱炎(AS)患者骨质疏松(OP)的发病机制。方法分别测定36例男性AS患者血清肿瘤坏死因子-a(TNF-a)、骨钙素(BGP)I、-型胶原C末端肽(CTX)水平及腰椎和股骨颈的骨密度(BMD)值,并与20例健康者对照。结果AS早期腰椎和股骨颈BMD均低于对照组,晚期股骨颈BMD更低于对照组。AS血清TNF-a、CTX水平较对照组显著增高(P<0.01;P<0.05),而血清BGP水平较对照组无显著差差异(P>0.05)。AS患者中OP组TNF-a、CTX水平较NOP组显著增高(P<0.01;P<0.05),OP组中血清TNF-a与CTX呈正相关,与股骨颈密度呈负相关;与BGP无明显相关性。结论AS患者主要是由于骨吸收增加而导致骨质疏松的发生。血清TNF-α水平的增高可促进骨吸收加强,是AS骨质疏松的重要原因之一。降低血清TNF-a水平,对AS患者骨质疏松的防治可能有积极的意义。     

绝经后肥胖女性骨密度与血管内皮功能的关系研究

目的 探讨绝经后肥胖女性中骨密度(BMD)与血管内皮功能的相关性.方法 选择自然绝经1～5年的单纯肥胖者(体重指数≥25kg/m2),年龄40～55岁,按照双能X线检测结果选择正常骨量组39例,骨量减少组37例和骨质疏松组19例.所有受试者测定体脂、BMD、骨矿含量(BMC)和血管内皮功能,包括血流介导的内皮依赖性血管舒张(EDD)和硝酸甘油介导的非内皮依赖性血管舒张.结果 骨质疏松组平均年龄和平均绝经时间显著高于正常骨量组和骨量减少组(P<0.05或P<0.01).骨质疏松组及骨量减少组BMD和BMC均显著低于正常骨量组(P<0.05或P<0.01).骨质疏松组EDD显著低于正常体重组和骨量减少组(分别为5.45±2.99、7.76±3.70和7.32±3.41,均P<0.05).相关分析显示各部位的BMD、BMC均与EDD相关(P<0.05和P<0.01).结论 肥胖女性绝经后骨质疏松与血管内皮功能异常有关,对绝经后肥胖女性低骨量人群干预治疗可能有助于防治动脉硬化及心血管疾病.     

老年男性糖尿病患者骨质疏松与动脉硬化的相关性研究

目的 探讨老年男性糖尿病人群骨质疏松与动脉硬化的相关性。方法 测定226例老年男性糖尿病患者的股骨近端骨密度（BMD）,将其分为骨质疏松组和非骨质疏松组,分别比较两组的一般情况,同时采用动脉硬化检测仪进行测定其踝肱指数（ABI）和脉搏波传导速度（PWV）。结果 骨质疏松组患者的吸烟比例较非骨质疏松组高,差异有显著性（P<0.05）。骨质疏松组患者的ABI显著低于非骨质疏松组,PWV高于骨质疏松组,两组比较差异有显著性（P<0.05）。随BMD水平下降,所有患者的PWV水平升高,ABI降低,提示动脉硬化程度加重。结论 老年男性糖尿病骨质疏松患者更易并发动脉粥样硬化病变,治疗和预防时应采取系统性的措施。