天然牛磺酸对高铅动物模型铅含量的影响

目的：探讨天然牛磺酸是否具有排铅解毒的作用.方法：[1]实验于2004-10/12在广西区疾病预防控制中心毒理科完成.选用SPF级Wistar纯种雄性大白鼠55只.将检疫合格大鼠按体质量分层随机分为5组：牛磺酸高、中、低3个剂量组（以纯牛磺酸计）,空白对照组,模型对照组,每组11只.[2]实验开始后,模型对照组、受试样品各剂量组每天饮用1g/L醋酸铅水溶液造模的同时,牛磺酸高、中、低剂量组动物灌胃给予纯牛磺酸0.07,0.14,0.21 mg/kg,1次/d,连续30 d;空白对照组不造成高铅模型,灌胃蒸馏水,灌胃量为10 mL/kg,1次/d,连续30 d.于末次给予受试药品24 h后.采用瞬间高压直流电550 V将大鼠电昏后处死,取血,取肝脏和股骨称重后进行湿式消化,用石墨炉原子吸收分光光度计测定铅含量.[3]计量资料差异.比较采用方差分析.结果：大白鼠55只均进入结果分析.[1]血铅水平：牛磺酸高、中、低剂量组均明显低于模型对照组[（2.49&;#177;0.31）,（2.54&;#177;0.27）,（2.40&;#177;0.29）,（3.45&;#177;0.88）μg/L,P＜0.01];模型对照组明显高于空白对照组[（0.38&;#177;0.18）μg/L,＜0.01].[2]肝组织铅含量：牛磺酸高、中、低剂量组均明显低于模型对照组[（1.73&;#177;0.64）,（1.51&;#177;0.16）,（1.45&;#177;0.63）,（2.40&;#177;0.43）μg/g,P＜0.01];模型对照组明显高于空白对照组[（0.45&;#177;0.10）μg/g,P＜0.01].股骨组织铅含量：牛磺酸高、中剂量组均明显低于模型对照组[（3.86&;#177;1.20）,（3.54&;#177;0.88）,（5.00&;#177;1.34）μg/g,P＜0.01];模型对照组明显高于空白对照组[（0.12&;#177;0.05）μg/g,P＜0.01].结论：天然牛磺酸具有促进血铅排出,降低肝组织、股骨内铅含量的作用.     

天然牛磺酸对高铅动物模型铅含量的影响

目的:探讨天然牛磺酸是否具有排铅解毒的作用。方法:①实验于2004-10/12在广西区疾病预防控制中心毒理科完成。选用SPF级Wistar纯种雄性大白鼠55只。将检疫合格大鼠按体质量分层随机分为5组:牛磺酸高、中、低3个剂量组(以纯牛磺酸计),空白对照组,模型对照组,每组11只。②实验开始后,模型对照组、受试样品各剂量组每天饮用1g/L醋酸铅水溶液造模的同时,牛磺酸高、中、低剂量组动物灌胃给予纯牛磺酸0.07,0.14,0.21mg/kg,1次/d,连续30d;空白对照组不造成高铅模型,灌胃蒸馏水,灌胃量为10mL/kg,1次/d,连续30d。于末次给予受试药品24h后。采用瞬间高压直流电550V将大鼠电昏后处死,取血,取肝脏和股骨称重后进行湿式消化,用石墨炉原子吸收分光光度计测定铅含量。③计量资料差异比较采用方差分析。结果:大白鼠55只均进入结果分析。①血铅水平:牛磺酸高、中、低剂量组均明显低于模型对照组犤(2.49±0.31),(2.54±0.27),(2.40±0.29),(3.45±0.88)μg/L,P<0.01犦;模型对照组明显高于空白对照组犤(0.38±0.18)μg/L,P<0.01犦。②肝组织铅含量:牛磺酸高、中、低剂量组均明显低于模型对照组犤(1.73±0.64),(1.51±0.16),(1.45±0.63),(2.40±0.43)μg/g,P<0.01犦;模型对照组明显高于空白对照组犤(0.45±0.10)μg/g,P<0.01犦。股骨组织铅含量:牛磺酸高、中剂量组均明显低于模型对照组犤(3.86±1.20),(3.54±0.88),(5.00±1.34)μg/g,P<0.01犦;模型对照组明显高于空白对照组犤(0.12±0.05)μg/g,P<0.01犦。结论:天然牛磺酸具有促进血铅排出,降低肝组织、股骨内铅含量的作用。     

牛磺酸复合液对运动员运动性疲劳的影响研究

[目的]通过观察牛磺酸复合液对专业运动员血液肝肾功能、相关酶学等生化指标的变化,探讨牛磺酸复合液抗运动性疲劳的效果.[方法]随机选取射击、射箭队男、女运动员各30名,分别分为对照组,实验组,对照组为空白对照,实验组服用"牛磺酸复合液",服法:口服,2次/天,1支/次.连续服用30 d.实验过程中,所有对象均按训练计划进行正常训练.运动员实验前均抽取清晨餐前静脉血,测定血中血尿素氮(BUN)、肌肝(CR)、肌酸激酶(CK)、超氧化物歧化酶(SOD)、尿酸(UA)、肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)、乳酶脱氢酶同工酶1(LDH-1)、脂质过氧化物丙二醛(MDA)、天冬氨酸转氨酶(AST)、丙氨酸转氨酶(ALT)、等各项指标,30 d后按同法抽取血样进行同样的测试.[结果]运动员服用本方剂后,血中SOD值的水平升高,而BUN、CR、CK、CK-MB、LDH、MDA则显著下降.[结论]牛磺酸复合液可通过清除组织自由基,来延缓运动性疲劳的发生,促进其恢复的作用.     

牛磺酸治疗高血压病的疗效及对血管内皮细胞功能的影响

目的观察牛磺酸对原发性高血压病(EH)病人的疗效及血管内皮活性物质内皮素1(ET-1)、血栓素A2(TXA2)、一氧化氮(NO)和降钙素基因相关肽(CGRP)的影响。方法56例EH病人用牛磺酸治疗2个月,观察用药前后血中ET-1、NO、CGRP和TXA2的变化。结果牛磺酸治疗EH总有效率为71.4%。牛磺酸治疗后血中NO、CGRP浓度均较治疗前显著升高(P<0.01),血中ET、TXA2浓度显著下降(P<0.01)。结论牛磺酸有较好的降压作用,可明显改善EH病人血管内皮功能。     

牛磺酸对慢性肾小球肾炎患者血小板活化因子水平的影响

目的　探讨牛磺酸对慢性肾小球肾炎患者血小板活化因子水平的影响及其对肾脏的保护作用。方法　用牛磺酸治疗 12例慢性肾小球肾炎患者 4周 ,采用生物活性法测定治疗前、后血浆及尿中血小板活化因子 (PAF)的含量 ,观察尿蛋白变化及临床表现。结果　经牛磺酸治疗后 ,慢性肾小球肾炎患者尿蛋白下降 ,血浆及尿中PAF显著减少。结论　牛磺酸能减轻慢性肾小球肾炎患者蛋白尿 ,降低血浆及尿中PAF水平 ,对慢性肾小球肾炎患者的肾脏有一定的保护作用     

牛磺酸对微囊化肝细胞生长的影响

目的：微胶囊中存在一定程度的高渗透压胁迫，可造成细胞生长代谢减慢，为改善微囊化肝细胞的生长，尝试应用抗渗透压胁迫物质牛磺酸，观察其对微囊化肝细胞生长的影响。方法：实验于2006-07／08在中国科学院大连化学物理研究所生物医学材料工程实验室完成。将HepG2细胞悬液（非微囊化细胞）和微囊化HepG2分别接种于牛磺酸浓度为0，0．6，0．8和1．2mmol／L的MEM培养液中，在37℃体积分数为0．05的CO2中培养。MTT法测定非微囊化和微囊化HepG2细胞的生长活性，相差显微镜观察囊内细胞生长状态。结果：①非微囊化HepG2细胞：0．6，0．8和1．2mmol／L的牛磺酸对其生长无影响，吸光度值比较差异无显著意义（P〉0．05）。②微囊化HepG2细胞：0．6，0．8mmol／L牛磺酸对微囊化肝细胞的生长亦无影响（P〉0．05）：但1．2mmol／L牛磺酸町以显著改善微囊化肝细胞的生长，其吸光度值高于0mmol／L牛磺酸组（P〈0．05），并促进细胞的聚集。结论：1．2mmol／L牛磺酸可以改善微囊化肝细胞的生长并抵制微囊内的高渗透压胁迫对细胞的生长抑制作用。     

牛磺酸对大鼠实验性呼吸窘迫综合征脂质过氧化的影响

用牛磺酸油酸引起的大鼠实验性呼吸窘迫综合征。占磺酸对肺系数、血浆ＭＤＡ、肺组织ＭＤＡ、ＳＣＤ及病理学改变等的影响。结果表明：牛磺酸可使肺系数减少，血浆肺组织ＭＤＡ含量降低（Ｐ〈０．０１），ＳＯＤ活性受到保护，肺组织病变减轻。提示：牛磺酸减轻肺损伤的作用与抗脂质过氧化有关。     

牛磺酸应用于冠心病康复的可行性研究：对运动大鼠血清脂质的影响

为观察牛磺酸应用于冠心病康复的可行性，我们研究了牛磺酸对运动大鼠血清脂质的影响。结果表明：运动＋牛磺酸组血清中牛磺酸深度较对照组、运动组都显著增加。与对照组比较，运动组血清中ＣＨ、ＬＤＬ显著降低，运动＋牛磺酸组ＣＨ、ＬＤＬ和ＴＧ都显著降低；、与运动组比较，运动＋牛磺酸组的ＴＧ显著降低，ＨＤＬ显著增加。提示牛磺酸可能使运动降血脂的作用更加完全而有效，牛磺酸在冠心病等与血脂有关疾病的预防、治疗和康复过     

探讨铅对孕激素的影响

目的:探讨重金属铅对女性孕激素的影响.方法:将在我院体检的女性体检者190例中确诊为高血铅的83例设为高铅组,血铅正常的107例设为对照组.观察两组的血铅值及对孕激素的影响.结果:高铅组体检者的孕激素为(3.77±2.73) nmol/L,对照组的孕激素为(6.64±2.37) nmol/L,两组比较有显著性差异(P＜0.05).且血铅浓度越高,对孕激素水平影响越大.结论:重金属铅对女性孕激素有影响.     

低水平铅暴露对婴儿的影响

目的 :探讨低水平铅暴露对一岁以内的婴儿体格发育、神经行为发育和铅、锌、铁、动态变化的影响。方法 :从我院 2 0 0 1年 3月～ 12月间出生的新生儿中选取 35例 ,以临主时孕妇血铅、婴儿血铅水平作为铅暴露指标。以身长、体重、头围作为体格发育指标 ;以锌、铁作为体内锌、铁变化的指标。在 3月± 1周、6月± 1周、9月± 1周、12月± 1周进行随访。结果 :孕妇血铅与婴儿血铅整呈正相关 ,孕妇血铅与 3、9个月婴儿血锌呈负相关。 3个月婴儿血锌和血铁有相关性。线性相关分析描示在临产孕妇血铅和 3、6、9个月婴儿血铅中有统计学意义。结论 :低水平铅暴露时婴儿神经行为发育造成不利影响 ;宫内铅和环境铅是影响出生后血铅水平的主要因素。提高血锌、铁水平可降低血铅水平。减少铅暴露的危害     

Effects of taurine on rat aorta in vitro

The effects of taurine on vascular tone of isolated thoracic aortic rings were investigated. We have observed that: 1) taurine is able to induce reduction of the basal contractile tone; 2) taurine exerts a relaxing action in artery segments preconstricted with high potassium medium noradrenaline; 3) the effect of taurine is either dependent on endothelium, nor mediated by adrenoceptors or muscarinic cholinoceptors; 4) in vessels with basal tone or in those preconstricted with noradrenaline, the presence of endothelium reduces the taurine-induced relaxation; 5) the actions of taurine are independent of extracellular calcium; 6) taurine increases the vasodilatation induced by a perfusion with a calcium-free medium. The physiological role of taurine in the maintenance of vascular tone in normal and pathological situations is discussed.     

健行颗粒对3种拟帕金森病震颤模型小鼠的干预作用

目的建立肌肉震颤及线粒体功能障碍致3种拟帕金森病震颤小鼠模型,并在此3种模型上观察健行颗粒的药效学作用,探讨其可能的作用机理.方法经氧化震颤素和槟榔碱单次腹腔注射建立小鼠肌肉震颤模型;经MPTP 20mg/kg连续8天腹腔注射建立线粒体损伤致震颤小鼠模型.记录震颤素和槟榔碱模型小鼠震颤持续时间;观察MPTP模型小鼠爬杆行为及自主活动次数的改变,经高效液相色谱测定MPTP模型小鼠纹状体内多巴胺及其代谢产物含量的改变.结果模型组小鼠在给予震颤素或槟榔碱腹腔注射后出现明显震颤,健行颗粒用药组小鼠震颤持续时间较模型组明显缩短;对于MPTP小鼠模型,模型组小鼠爬杆时间延长,运动协调性降低,纹状体内多巴胺含量明显降低,健行颗粒用药组小鼠爬杆时间较模型组明显缩短,自主活动数增加,纹状体内多巴胺含量增高.结论槟榔碱及氧化震颤素均能制备良好的肌肉震颤小鼠模型,健行颗粒能明显减少模型动物肌肉震颤持续时间;对于MPTP腹腔注射拟帕金森小鼠模型,健行颗粒能明显缩短其爬杆时间,增强小鼠自主活动能力,提升小鼠脑纹状体内多巴胺及其代谢产物的含量.     

Potential therapeutic action of natural products from traditional Chinese medicine on Alzheimer's disease animal models targeting neurotrophic factors

Alzheimer's disease (AD) is a neurodegenerative disorder in which the death of brain cells leads to memory loss and cognitive decline. To reduce the death rate and improve the biological activity of neurocytes, neurotrophic factors (NTFs) exhibit therapeutic effect on AD. However, therapeutic application of exogenous NTFs in treatment of AD is largely limited due to short half‐life, poor stability, etc. Various extracts of traditional Chinese medicine (TCM) have been shown to exhibit therapeutic effects on AD, and some of these effects are associated with regulation on the expression of nerve growth factor, brain‐derived neurotrophic factor (BDNF), and glial cell line‐derived neurotrophic factor (GDNF) and their associated receptors. This article reviews the progress on promotion of Panax ginseng, Rehmannia glutinosa Libosch., Epimedium, Polygala tenuifolia Willd, and seven other TCMs on secretion of NTFs during AD, with a view to preparation development and clinical application of these TCMs on AD.     

Putting the bio in biobehavioral: animal models

Animal models are useful in research that examines physiological mechanisms and, as such, are invaluable in developing therapies to alleviate illness and promote health. Ethical considerations are essential for proper animal use and include replacement by nonanimal models where possible, reduction in the numbers of animals used, and refinement of experimental protocols to reduce animal suffering. Choosing the optimum model depends on the long- and short-term goals of the project, and the choice of a model goes hand in hand with appropriate study design. Five key features to think about when choosing a model are as follows: model asymmetry, necessary differences, specificity to the study, model validity, and model improvement. Appropriate use of both male and female animals has also become an important issue in recent times. These considerations will assist in understanding animal model use.     

Lessons on autoimmune diabetes from animal models

T1DM (Type I diabetes mellitus) results from selective destruction of the insulin-producing beta-cells of the pancreas by the immune system, and is characterized by hyperglycaemia and vascular complications arising from suboptimal control of blood glucose levels. The discovery of animal models of T1DM in the late 1970s and early 1980s, particularly the NOD (non-obese diabetic) mouse and the BB (BioBreeding) diabetes-prone rat, had a fundamental impact on our ability to understand the genetics, aetiology and pathogenesis of this disease. NOD and BB diabetes-prone rats spontaneously develop a form of diabetes that closely resembles the human counterpart. Early studies of these animals quickly led to the realization that T1DM is caused by autoreactive T-lymphocytes and revealed that the development of T1DM is controlled by numerous polymorphic genetic elements that are scattered throughout the genome. The development of transgenic and gene-targeting technologies during the 1980s allowed the generation of models of T1DM of reduced genetic and pathogenic complexity, and a more detailed understanding of the immunogenetics of T1DM. In this review, we summarize the contribution of studies in animal models of T1DM to our current understanding of four fundamental aspects of T1DM: (i) the nature of genetic elements affording T1DM susceptibility or resistance; (ii) the mechanisms underlying the development and recruitment of pathogenic autoreactive T-cells; (iii) the identity of islet antigens that contribute to the initiation and/or progression of islet inflammation and beta-cell destruction; and (iv) the design of avenues for therapeutic intervention that are rooted in the knowledge gained from studies of animal models. Development of new animal models will ensure continued progress in these four areas.     

神经干细胞移植对帕金森病鼠纹状体多巴胺含量的影响

目的观察神经干细胞定向移植后对帕金森鼠纹状体多巴胺含量的影响,证实神经干细胞移植治疗的可行性。方法建立帕金森病模型大鼠以及体外培养神经干细胞,然后将神经干细胞悬液立体定向移植到帕金森病模型鼠黑质纹状体区,测定纹状体的多巴胺含量,并与生理盐水组和非移植组相比。结果神经干细胞移植后帕金森病模型鼠纹状体多巴胺含量(346±26)μg/g与生理盐水组(58±56)μg/g和非移植组(72±60)μg/g比较明显增多,经t检验差异有显著性意义(t=13.99,12.57,P<0.05)。结论神经干细胞移植能减轻6-羟基多巴胺对黑质纹状体多巴胺能神经元的损伤。