中国雪蛤酶解液预防去卵巢大鼠骨质疏松

背景：以往研究发现雪蛤具有预防绝经后相关疾病的作用,但是否具有预防绝经后骨质疏松的功效有待于深入研究。 目的：验证雪蛤酶解液对去卵巢大鼠骨质疏松的预防作用。 方法：健康成年Wistar大鼠72只,按随机数字表法分为6组,每组12只。假手术组大鼠不切除卵巢仅切除卵巢周围部分脂肪,其余各组均切除卵巢造成骨质疏松模型。于造模后第7天开始,各组等容灌胃,连续12周。假手术组和模型组每日灌胃等量蒸馏水;普雷马林组每日灌胃387.8 g/L普雷马林(结合雌激素片)悬浮液6. 67 g/(kg•d);67.0,26.8,13.4 g/(kg•d) 蛤士蟆酶解液组每日分别按相应剂量灌胃。每个月测定食物利用率;实验12周末时,处死大鼠后取子宫,测定子宫质量;取左、右侧股骨和腰椎骨,双能X射线骨密度仪测定骨密度;电感偶合等离子体直读光谱仪测定骨钙、磷含量;脱脂、灰化后测定骨干质量、灰质量。 结果与结论：在4组干预组中,67.0 g/(kg•d)蛤士蟆酶解液组和普雷马林组的食物利用率最低(P < 0.05);在各切卵巢组中,普雷马林组的子宫质量最重(P < 0.05);26.8 g/(kg•d) 蛤士蟆酶解液和普雷马林可以延缓切卵巢大鼠股骨骨密度的下降(P < 0.05);67.0,26.8,13.4 g/(kg•d)蛤士蟆酶解液组骨钙和骨磷与模型组比较均有明显提升(P < 0.05),与普雷马林组差异无显著性意义(P > 0.05)。提示雪蛤酶解液对去卵巢大鼠的骨质疏松具有预防作用,其疗效与结合雌激素片相当,且对子宫增生的不良反应低于结合雌激素片。     

中药联合胰岛素预防糖尿病去卵巢大鼠骨质疏松症

目的研究中药对糖尿病并发去卵巢大鼠骨质疏松症的影响。方法80只雌性Wistar大鼠随机平均分为4组：假手术组（A组）、糖尿病假手术组（B组）、糖尿病去卵巢组（C组）和糖尿病去卵巢中药干预组（D组）,造模成功12周后应用双能X线骨密度仪测定骨密度。结果L5、L4椎体骨密度在各组的数值变化关系：A组〉D组〉B组〉C组。其中,L5椎体骨密度D组与A、B、C组相比差异均具有统计学意义（P〈0．01或P〈0．05）;L5椎体骨密度D组与A、C组相比差异均具有统计学意义（P〈O．01）,D组与B组相比差异无统计学意义（P〉0．05）。股骨的骨密度D组与A组相比差异无统计学意义（P〉0．05）,与C组相比差异具有统计学意义（P〈0．01）。结论补肾中药结合胰岛素治疗可预防糖尿病去卵巢大鼠骨质疏松模型。     

构建动脉粥样硬化模型大鼠升主动脉的应力松弛曲线

背景：动脉粥样硬化的起因尚无定论，但和血管血流时的应力变化有关。 目的：比较正常和动脉粥样硬化动物模型升主动脉的应力松弛流变特性，确定动脉粥样硬化对升主动脉应力松弛特性的影响。 设计、时间及地点：随机对照实验，于2008-12-16/30在吉林大学力学实验中心完成。 材料：普通级雄性4月龄SD大鼠20只，体质量165~200 g，随机分成正常对照10只，模型组10只，参考文献复制动脉粥样硬化模型。 方法：两组大鼠饲养4周后处死，取出大鼠升主动脉，密封后置于-20 ℃冰箱内保存备用。实验前取出标本，常温下解冻，切取试样。在日本岛津电子万能试验机上对正常对照和模型组各8个试样进行应力松驰实验。应力松弛实验的应变增加速度为5%/s。设定实验时间为7 200 s，采集100个数，以一元线性回归分析的方法处理实验数据。 主要观察指标：①应力松弛曲线和数据。②归一化应力松驰函数方程的计算。 结果：正常对照和模型组升主动脉应力松弛最初600 s变化较快，之后应力缓慢下降，正常对照组7 200 s应力松弛量 1.5 MPa，模型组7 200 s应力松弛量0.856 MPa。 结论：应力松弛曲线是以对数关系变化的，动脉粥样硬化对升主动脉应力松弛特性具有一定影响。     

骨性关节炎动物模型内侧副韧带的应力松弛☆

背景：韧带和其他生物软组织一样,具有黏弹性特性,其应力松弛和蠕变黏弹性特性是为适应人的生理功能需要而存在的。研究说明骨性关节炎对韧带力学性能具有一定影响。 目的：比较正常和骨性关节炎动物模型内侧副韧带的应力松弛流变特性,确定骨性关节炎对内侧副韧带应力松弛特性的影响。 方法：以闭合关节刻痕法复制骨性关节炎动物模型,取正常和骨性关节炎动物模型大鼠膝关节内侧副韧带各10个试样,进行应力松弛实验。应力松弛实验的应变增加速度为5%/s。设定实验时间为7 200 s,采集100个数据,观察应力松弛数据和曲线、应力与时间的变化规律,以一元线性回归分析的方法处理实验数据。 结果与结论：正常组和病态组试样应力松弛最初600 s变化较快,之后应力缓慢下降,正常组7 200 s应力松弛量0.47 MPa,病态组7 200 s应力松弛量0.29 MPa。模型组7 200 s应力松弛量显著低于正常组(P < 0.05),且应力松弛曲线是以对数关系变化的。说明骨性关节炎时可以使膝关节对内侧副韧带应力松弛量降低,对膝关节应力松弛特性具有一定影响。     

去卵巢、去松果体对大鼠杏仁核细胞凋亡的影响

阿尔茨海默病(Alzheimer’s disease，AD)临床主要表现为记忆力减退，其中受情绪影响的长时记忆减退主要与杏仁核的神经元减少有关。AD的病因至今不清，近来研究结果显示，体内雌激素(estrogen，E)、褪黑素(melatonin，MT)缺乏与AD发病有关，而细胞凋亡可能参与了发病过程心。     

骨质疏松大鼠MSCs生物学特性的研究

背景：随着近年来对骨质疏松机制研究的深入,研究者逐渐把研究重点放在了成骨细胞的来源骨髓间充质干细胞上。目的：对骨质疏松大鼠骨髓间充质干细胞进行分离和体外培养,观察骨质疏松模型大鼠骨髓间充质干细胞的生物学特性,分析骨质疏松的细胞病理学机制,以期为骨质疏松的防治提供一个有意义的药物靶标。方法：选用10月龄SD雌性大鼠去卵巢增龄3个月来复制骨质疏松模型,设假手术对照组。运用密度梯度离心法对两组大鼠骨髓间充质干细胞进行分离和体外培养,运用扫描电镜对培养的骨髓间充质干细胞进行形态学观察,并行生长曲线及贴壁率检测。结果与结论：骨质疏松大鼠的骨髓间充质干细胞增殖能力明显下降,与对照大鼠相比存在许多结构特征的差异。体外实验结果表明,骨质疏松大鼠骨髓间充质干细胞的体外增殖能力下降可能是骨质疏松的细胞病理学机制。关键词：间充质干细胞;骨质疏松;去卵巢素;大鼠;贴壁率     

去卵巢大鼠下丘脑-垂体-卵巢轴的功能代偿机制研究

目的：在细胞和分子水平上，探讨机体因各种原因导致卵巢功能低下时，下丘脑-垂体-卵巢轴(HPOA)功能的自然代偿机制。方法：观察大鼠切除卵巢后1～6个月，下丘脑促性腺激素释放激素(Gonadotmpin releasing hormone，GnRH)及其mRNA表达的改变以及阴道脱落细胞形态和外周血雌二醇(E2)水平的变化。结果：去卵巢后5～6个月时，大鼠阴道涂片出现成熟脱落细胞；4个月时血E2水平明显升高，6个月时几乎稳定在正常水平的一半以上；随去卵巢时间延长，大鼠下丘脑GnRH神经元数目较去卵巢1个月时逐渐增多，至6个月时，升高有显著差异，但仍低于正常组数目；去卵巢1个月大鼠下丘脑组织GnRHmRNA表达明显减少，去卵巢后5个月明显升高，与正常组相比没有显著差异；GnRH棘型神经元的比例在去卵巢4个月时即升高到正常水平。结论：大鼠卵巢功能低下时，机体体内可能存在一种自然代偿作用，使异常的HPOA功能趋于正常化。     

手指屈肌腱应力松弛的蠕变实验

背景：屈肌腱损伤都要进行吻接修复。 目的：通过实验定量得出手指屈肌腱应力松弛和蠕变与时间的变化规律,为人工屈肌腱和临床外科吻接术提供黏弹性力学参数。 设计、时间及地点：单因素实验,于2006-06-20/30在吉林大学力学实验中心完成。 材料：实验标本取自正常国人急性头部创伤致死的新鲜尸体4具由白求恩医科大学解剖教研室提供,均为男性,年龄19~28岁。于死亡2 h之内解剖尸体取下屈肌腱。 方法：在日本岛津电子万能试验机上对手指屈肌腱各8个试样进行应力松弛、蠕变实验。模拟人体体温36.5 ℃的温度场下进行实验,应力松弛的应变增加速度为5%/s,蠕变实验的应力增加速度为0.05 GPa/min。设定实验时间为7 200 s,采集100个数据以一元线性回归分析的方法处理实验数据。 主要观察指标：①应力松弛曲线。②归一化应力松弛函数方程的计算。③蠕变实验曲线结果。④归一化蠕变函数方程计算结果。 结果：手指屈肌腱应力松弛、蠕变最初600 s变化较快,之后应力缓慢下降,应变缓慢上升,7 200 s应力松弛量为0.219 MPa,7 200 s蠕变量为3.1%。 结论：应力松弛曲线是以对数关系变化的,蠕变曲线是以指数关系变化的,其具有很好的黏弹性力学特性。     

去卵巢、去松果体对大鼠隔区细胞凋亡的影响

近来有些学者认为[1,2 ] 老年期体内雌激素(Estrogen ,E)、褪黑素(Melatonin ,MT)水平下降是老年疾病中的危险因素。研究显示阿尔茨海默病(Alzheinmer,sdisease ,AD)患者的边缘系统存在着广泛性萎缩,其中最大百分比的体积丧失出现在隔区(34% ) ,并且隔区的病理损害与AD的情绪障碍、学习与记忆能力减退密切相关[3] 。隔区参与了情感反应及学习记忆活动的神经环路。关于E、MT与隔区病理损害关系的研究较少,本实验通过给大鼠去卵巢(Ovariectomy ,OVX)、去松果体(Pinealectomy ,PX) ,造成内源性E、MT缺乏,观察隔区病理损害情况,以了解…     

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。     

雌激素与辛伐他汀序贯法干预对去势大鼠骨质疏松的治疗作用

背景：Frost根据骨重建的概念创建了骨重建干预理论——序贯疗法,即在骨吸收抑制剂之后可给予刺激骨形成的药物。 目的：基于骨重建干预理论,序贯应用雌激素与辛伐他汀干预骨重建吸收期和形成期,观察其对去势大鼠骨质疏松的治疗作用。 方法：3月龄雄性SD大鼠40只,以随机数字表法分为去势组与正常对照组。去势组切除双侧卵巢,正常对照组只进行下腹部皮肤单纯切开术。大鼠去势后1个月,将去势组随机分为3组：序贯组、雌激素组、去势对照组,并开始药物干预：序贯组,皮下注射苯甲酸雌二醇0.1 mg/kg,3 d给药1次,2周后,灌胃给予辛伐他汀5 mg/(kg•d)2周,停药5周,再应用辛伐他汀5 mg/(kg•d)灌胃2周;雌激素组,皮下注射苯甲酸雌二醇0.1 mg/kg,每3 d给药1次,连续用药11周;去势对照组,单纯的饲料喂养,无药物干预。11周后,双能X射线骨密度仪测定股骨骨密度,放射免疫法检测血清白细胞介素6、骨钙素水平。 结果与结论：各治疗组大鼠股骨骨密度、骨钙素水平高于去势对照组(P < 0.05),并且序贯组明显高于雌激素组(P < 0.05)。各治疗组白细胞介素6水平低于去势对照组(P < 0.05),并且序贯组低于雌激素组(P < 0.05)。说明雌激素和辛伐他汀序贯疗法可以通过抑制骨吸收,促进骨形成有效地治疗骨质疏松。     

补肾健脾方干预去势大鼠骨骼肌caspase-3和caspase-8的表达

背景：骨骼肌与骨质疏松症关系密切,导致其衰退的主要原因是细胞的凋亡,这种凋亡可能是Caspase家族蛋白所介导的。 目的：探讨补肾健脾方对去势大鼠骨骼肌caspase-3和 caspase-8调控作用。 方法：SD大鼠48只等随机分为对照组、模型组、中药组、西药组,后3组大鼠摘除双侧卵巢建立骨质疏松模型,对照组仅切除周围少量脂肪组织。造模2周后,中药组给予补肾健脾方(2.979 g/kg)灌胃,西药组给予戊酸雌二醇片(0.104 mg/kg)灌胃,模型组和对照组给予蒸馏水灌胃,1次/d。 结果与结论：①干预12周后,双能X线骨密度仪测量发现,相比于对照组,模型组大鼠左侧股骨的骨密度值和骨矿含量均明显降低(P < 0.01);而中药组和西药组的骨密度值均高于模型组(P < 0.05),且2组骨密度值和骨矿含量接近(P > 0.05)。②酶标免疫分析显示,与对照组相比,模型组骨骼肌中Caspase-3和 Caspase-8表达水平明显上升(P < 0.05)。中药能显著降低大鼠骨骼肌中Caspase-3的表达水平(P < 0.05),而西药能显著减低Caspase-8表达水平(P < 0.05)。③说明补肾健脾方对卵巢切除所致的骨质疏松症有明显的治疗作用,能明显提高骨密度,而且能显著减低Caspase-3的水平,但不能显著减低Caspase-8水平,显示补肾健脾方不是通过死亡受体途径去抑制细胞凋亡的。     

The effects of stimulation and lesion of raphe nuclei on luteinizing hormone release in estrogen-progesterone-treated ovariectomized rats

A study was made of the effects of electrochemically stimulating (ECS) and destroying the midbrain dorsal and median raphe nuclei on the estrogen-progesterone- (EP) induced surge of pituitary LH release in ovariectomized rats. ECS and lesions were produced simultaneously with anodal direct current through a chronically implanted stimulation-lesion electrode. Blood for LH assay was collected through a chronic intra-atrial cannula positioned on the day of first treatment with progesterone. ECS of the raphe nuclei exerted a strong inhibition of the LH surge when compared with sham stimulation. On the second EP treatment the onset of the LH surge was advanced both in sham-stimulated animals and in rats with raphe lesions resulting from the anodal direct current of the initial ECS. It was suggested that this apparent facilitation of the LH surge on the second EP treatment was the result of reduced stress or an altered hormonal milieu and not a consequence of destroying the raphe nuclei. The results confirm in a chronic preparation that stimulation of raphe nuclei depresses the EP-induced LH surge and that subsequently in the absence of the raphe nuclei the LH response to EP treatment is apparently normal.     

Effects of genistein on neuronal apoptosis, and expression of Bcl-2 and Bax proteins in the hippocampus of ovariectomized rats

Genistein is one of several isoflavones that has a structure similar to 17β-estradiol, has a strong antioxidant effect, and a high affinity to estrogen receptors. At 15 weeks after ovariectomy, the expression of Bcl-2 in the hippocampus of rats decreased and Bax expression increased, with an obvious upregulation of apoptosis. However, intraperitoneal injection of genistein or 17β-estradiol for 15 consecutive weeks from the second day after operation upregulated Bcl-2 protein expression downregulated Bax protein expression, and attenuated hippocampal neuron apoptosis. Our experimental findings indicate that long-term intervention with genistein can lead to a decrease in apoptosis in hippocampal neurons following ovariectomy, upregulate the expression of Bcl-2, and downregulate the expression of Bax. In addition, genistein and 17β-estradiol play equal anti-apoptotic and neuroprotective roles.     

The short latency muscle reflex in the diagnosis of disc disease affecting roots L4 and L5

A segmental monosynaptic reflex that can be evoked by using voluntary muscle contraction to facilitate it is of use in diagnosis. In a group of 15 healthy volunteers the reflex response from tibialis anterior proved to be 31.08±2.48 msec with a side difference of 0.41±0.36 msec and from peroneus longus 29.90±2.20 msec with a side difference of 0.38±0.25 msec. Of 21 patients with radiologically proven disc herniation (of root L4 in 5 and of root L5 in 16) 16 showed a delay of more than 2.5 SD of the side difference or no response at all. It is hope that this simple and speedy method will be routinely adopted as complement to standard electromyography.

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Sommario Un riflesso segmentario monosinaptico può essere evocato facilitandone la risposta attraverso una contrazione volontaria muscolare. La risposta riflessa dal mscolo Tibiale Anteriore (T.A.) è risultata in un gruppo di 15 volontari sani, 31.08+/–2.48 msec. con una differenza di lato di 0.41+/–0.36 msec. Dal Peroneo Lungo (P.L.) 29.90+/–2.20 msec. con differenza di lato di 0.38+/–0.25 msec. In un gruppo di 21 soggetti affetti da ernia discale, radiologicamente provata, (in 5 della radice L4, in 16 della radice L5) abbiamo riscontrato un ritardo oltre le 2.5 SD della differenza di lato o una assenza di risposta in 16 casi su 21. Data la semplicità e la rapidità della metodica se ne auspica un utilizzo routinario come completamento di una indagine elettromiografica convenzionale.

     

TLR4、MRP8在内侧颞叶癫痫幼大鼠海马中表达的动态变化

目的观察氯化锂-匹罗卡品致痫幼大鼠各期海马中Toll-样受体4(TLR4)、髓样相关蛋白8(MRP8)表达的变化,探讨其是否与内侧颞叶癫痫(MTLE)发生有关。方法 21d SD雄性大鼠90只,随机分对照组(30只)和模型组(60只),腹腔注射氯化锂。17～18h后模型组腹腔注射匹罗卡品诱导癫痫持续状态(SE);对照组予等量生理盐水取代匹罗卡品腹腔注射。按自发发作出现和稳定时间(自发痫性发作在致痫后约3w出现,8w趋稳定),对照组和模型组随机分6个亚组:急性模型组(SE后2h)、潜伏模型组(SE后3w)、慢性自发发作组(SE后8w)及相对应时间点对照组。每亚组动物10只。免疫组化、免疫印迹、RT-PCR技术测定各亚组幼大鼠海马内TLR4、MRP8的表达。结果 TLR4、MRP8在模型组海马内表达明显增多,以CA3、CA1、DG区显著;与对照组相比,差异有显著性(P0.05)。模型亚组内,TLR4、MRP8在急性期和慢性期表达明显增高,而潜伏期无明显表达变化;3组比较差异有显著性(P0.05)。结论大鼠海马内TLR4、MRP8表达增多可能与MTLE发生有关。探讨其机制可能为MTLE的治疗提供新的靶点。     

骨质疏松性牙周炎大鼠左归丸与雌激素治疗后颌骨结构和骨量的变化*◆

背景：有研究表明经典补肾方剂左归丸可用于治疗绝经后女性的骨质疏松。 目的：观察骨质疏松性牙周炎大鼠左归丸与雌激素治疗后颌骨结构和骨量的变化。 方法：将SD大鼠麻醉下结扎上颌第一磨牙建立牙周炎模型、摘除大鼠卵巢建立骨质疏松模型,去势3个月后分别用左归丸和戊酸雌二醇治疗3个月。 结果与结论：左归丸、戊酸雌二醇治疗均能促进大鼠牙槽骨的新生,减轻牙周附着丧失(P < 0.05),使破骨细胞数量减少 (P < 0.05),牙周组织中骨保护素水平升高(P < 0.01),降低了血清中的碱性磷酸酶水平(P < 0.01)。结果证实,左归丸、戊酸雌二醇在改善骨质疏松性牙周炎大鼠牙槽骨结构的基础上,促使颌骨骨量增加。     

Evidence for S284L mutation of the CHRNA4 in a white family with autosomal dominant nocturnal frontal lobe epilepsy

PURPOSE: To identify mutations of the neuronal nicotinic acetylcholine receptor alpha4 subunit gene (CHRNA4) responsible for autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) in a group of white patients. METHODS: A group of 47 patients from 21 unrelated families with ADNFLE were screened for mutations in CHRNA4. Clinical features and EEG findings in the patients were consistent with those reported in the literature for other affected families. The entire gene was amplified from genomic DNA by polymerase chain reaction (PCR) followed by multitemperature single-strand conformation polymorphism analysis (MSSCP) and sequencing. RESULTS: A c.851C>T transition in exon 5 of CHRNA4 was identified in three affected individuals from two generations of the same family, but not in the remaining patients or in 100 healthy volunteers. This mutation caused an S284L substitution in the transmembrane domain M2 segment of the alpha4 subunit of the neuronal nicotinic acetylcholine receptor. The same mutation had previously been detected in a single Japanese family with ADNFLE, and in an Australian woman with a sporadic form of NFLE. CONCLUSIONS: This is the first report of an occurrence of c.851C>T transition in a white family with ADNFLE.     

Anatomical evidence that the uninjured adjacent L4 nerve plays a significant role in the development of peripheral neuropathic pain after L5 spinal nerve ligation in rats

Rats develop hyperalgesia and allodynia in the hind paw after L5 spinal nerve ligation. Phosphorylated extracellular regulated kinase (pERK) was used as a pain marker to investigate the potential role of adjacent uninjured L4 nerve in the development of heat hyperalgesia after L5 nerve injury. Left L5 nerve was ligated and sectioned in rats. Three days later, rats were randomly assigned to five groups; each had both hind paws immersed in water at different temperatures (no heat, 37, 42, 47, and 52°C) under sevoflurane anesthesia for 2 minutes. Five minutes after stimulation the rats were sacrificed and sections of L3–L6 spinal segments were stained immunocytochemically with pERK antibody. pERK immunoreactivity, which is not detectable in the normal spinal cord, was discernible in neurons (not glia) of the superficial dorsal horn after noxious heat stimuli. pERK‐positive neurons clearly overlapped in laminae I–II with normal unmyelinated and thin myelinated afferents labeled with calcitonin gene‐related peptide and isolectin B4, and injured unmyelinated afferents labeled with vasoactive intestinal polypeptide. There was a linear increase in pERK immunoreactivity on both sides with an increase in temperature. Importantly, the number of positive pERK neurons was significantly higher in the ipsilateral side of L4 spinal segment, which receives innervation from uninjured L4 nerve, compared with the contralateral control side, which receives both uninjured L4 and L5 spinal nerves. The data demonstrate that the uninjured L4 nerve plays an important role in the development of heat hyperalgesia at the spinal cord level after L5 nerve injury. J. Comp. Neurol. 523:1731–1747, 2015. © 2015 Wiley Periodicals, Inc.