牛磺酸对大鼠心肌损伤时心肌细胞核钙转运功能异常的保护作用

目的观察异丙肾上腺素 (ISO)致大鼠心肌缺血损伤时心肌细胞核钙转运功能的异常变化及牛磺酸对其影响。方法给Wister大鼠皮下注射5mg·kg-1ISO液 ,造成心肌缺血损伤模型。超速离心分离纯化心肌细胞核。酶学方法鉴定核纯度和测定核膜Ca 2 _ATP酶活性 ,同位素法观测核钙的摄取。结果与正常对照组比较 ,心肌缺血组 (实验组 )心肌细胞核膜钙依赖性ATPase活性降低18.1 % (P<0.05) ,45Ca2 摄取效率也显著降低 ,其最大速度降低54.6 % ;牛磺酸保护组心肌细胞核Ca2 _ATPase活性及核45Ca2 摄取与正常对照组比较均未见显著性改变。结论牛磺酸对ISO致大鼠心肌损伤时心肌细胞核钙转运功能降低有保护作用     

实验性犬脑干缺血模型牛磺酸含量及PLA2活性的动态变化

目的：观察犬脑干持续缺血后Tau含量及磷脂酶A2（PLA2）活性的动态变化，探讨脑干缺血时Tau的神经保护作用及PLA2的激活情况。方法：建立犬脑干缺血模型，动态观察缺血后各时点脑干组织中Tau含量（应用美国Beckman公司生产的6300黄金系列高效氨基酸分析仪测定）及PLA2活性（微量酸滴定法）的改变，同时观察神经元病理损害情况。结果：与假手术组相比，缺血30min，Tau含量显著增加（P＜0．05），PLA2活性亦显著增高（P＜0．05），神经元轻度异常；缺血3h,Tau含量增加更显著（P＜0．01），PLA2活性非常显著升高（P＜0．01），神经元呈中度缺血改变；缺血6－12h，Tau含量及PLA2活性仍继续增高（P＜0．01),神经元呈重度缺血改变或死亡。结论：脑干持续缺血后Tau的含量及PLA2的活性不断增高；Tau可能在脑干缺血早期起神经保护作用。     

牛磺酸治疗糖尿病大鼠骨骼肌病变的实验研究

目的：研究牛磺酸对糖尿病大鼠骨骼肌酶的影响。方法：SD大鼠24只，随机分为对照（NC）组、糖尿病（DM）组、牛磺酸（Tau）组，每组8只：DM组和Tau组腹腔注射链脲菌素（STZ）50mg／kg复制DM大鼠模型。NC组和DM组给予自来水、Tau组给予牛磺酸（1％饮水）4周后，测量腓肠肌组织中的乳酸脱氢酶（LDH）、超氧化物歧化酶（SOD）、肌酸激酶（CK）的活性及丙二醛（MDA）含量的变化；光镜下观察肌纤维病理改变。结果：与NC组相比，DM组组织中SOD、CK活性显著降低（P〈0．01），LDH活性、MDA含量显著增加（P〈0．01）；光镜下，肌纤维发生明显紊乱。变细，甚至断裂。给予牛磺酸后可抑制上述现象。结论：牛磺酸对糖尿病大鼠骨骼肌病变有保护作用。     

Taurine uptake by chick embryo retinal neurons and glial cells in purified culture

The properties and cellular distribution of a high-affinity uptake mechanism for taurine have been investigated using separate populations of purified chick embryo neural retina neurons and glia. Purified neuronal monolayers, cultured in serum-free medium, were incubated in radioactive taurine under different conditions and studied autoradiographically and biochemically. Labeling with radioactive taurine was detected in the perikaryon of most of the neurons present in the cultures. Neuronal uptake occurred by means of a high-affinity mechanism which was completely inhibited at low temperatures or in the absence of sodium ions. The uptake was linear for at least 1 hr and, as is the case in vivo, could be inhibited by gamma-aminobutyric acid (GABA) or beta-alanine. Incubation in ouabain, glutamate, or high K+ concentrations failed to cause any increase in the amount of taurine released by neurons preloaded with the radioactive amino acid. The rather wide-spread distribution of high-affinity taurine uptake was confirmed using separate retinal cultures rich in glial cells. Practically 100% of the glial cells appeared labeled after incubation in 10(-7) M [3H] taurine, and this uptake was also inhibited by low-temperature, Na+-free medium, GABA, or beta-alanine. Several pieces of evidence indicate that high-affinity taurine uptake coexists with uptake mechanisms for other amino acids, such as GABA, glutamate, and aspartate, in retinal neurons as well as glial cells. These in vitro populations offer a promising experimental system for the investigation of the effects of taurine on retinal cells.