牛磺酸治疗早产儿全静脉营养胆汁淤积的疗效

目的　观察早产儿应用全静脉营养后是否出现胆汁淤积 ,并探讨牛磺酸治疗胆汁淤积的效果。方法　将小于 33周的早产儿分为甲乙两组 ,均行全静脉营养 ,甲组应用牛磺酸治疗 ,乙组未应用牛磺酸治疗 ,并与大于 33周早产儿及足月儿对照 ,入院后第 1、7、14、2 1天采血测定丙氨酸转氨酶、直接胆红素、γ谷氨酰转肽酶。结果　入院后第 14、2 1天甲乙两组直接胆红素、γ谷氨酰转肽酶显著高于大于 33周的早产儿及足月儿 ,各时段甲乙两组 3项指标无显著差异。结论　较长时间全静脉营养可致胆汁淤积 ,牛磺酸对胆汁淤积治疗无明显效果 ,表明全静脉营养导致胆汁淤积原因的复杂性     

牛磺酸对染铅大鼠海马一氧化氮合酶活力的影响

目的　探讨牛磺酸拮抗铅损害学习记忆能力的作用。方法　采用NADPH d组织化学法 ,研究饮用含不同剂量铅 (0 .0 11、0 .110g L)的水和含不同剂量牛磺酸 (5、10g kg)的饲料喂养的大鼠海马一氧化氮合酶 (NOS)阳性神经元数量的变化。结果　 10g kg的牛磺酸饲料能明显增加染铅大鼠海马CA1区和齿状回NOS阳性神经元的数量。低铅水高牛磺酸饲料组NADPH d阳性神经数量在CA1区为 5 1.80± 4 .6 8,在齿状回为 4 7.4 0± 4 .2 0 ,较低铅水普通饲料组的CA1区 (4 1.2 0± 5 .32 )和齿状回 (39.87± 3.81)明显增多 ,差异有显著性 (P <0 .0 5 )。结论　牛磺酸对铅损害学习记忆能力有较明显的拮抗作用。     

体外冲击波碎石术损伤肾脏的氧化应激机制研究及牛磺酸的改善作用

目的:本文探讨体外冲击波碎石术损伤肾脏的氧化应激机制研究及牛磺酸的改善作用.方法:对本院80例肾结石行体外冲击波碎石术患者进行分析.所有患者随机分为两组:牛磺酸组于体外冲击波碎石术前1d口服牛磺酸粉,安慰剂组服用安慰剂,维持7d(2 g/次,tid).分析两组术后微量蛋白尿、β2-微球蛋白、丙二醛(MDA)及谷胱甘肽过氧化物酶(GSH-Px)水平变化.Western Blotting法分析NOX2、NOX4及肿瘤坏死因子α(TNF-α)的表达变化.以健康体检者为对照组.结果:与对照组相比,冲击波碎石后微量蛋白尿、β2-微球蛋白、MDA水平明显增高SOD及GSH-px水平和Bcl2明显降低,而NOX2/4、Bax及TNF-α的蛋白表达明显增强.牛磺酸组的上述指标得到部分恢复.结论:牛磺酸通过抑制氧化应激反应和细胞凋亡减弱体外冲击波碎石术对肾脏的损伤作用.     

牛磺酸对外源性羟自由基诱导心肌细胞凋亡的影响

目的：观察牛磺酸对外源性羟自由基诱导心肌细胞凋亡的影响。方法：采用培养的第2代心肌细胞，随机分面4组：（1）正常对照组：仅用DMEM培养；（2）羟自由基组：OH－终浓度为0．1mmol.L^-1；（3）牛左酸组：牛磺酸终浓度为30mmol.L^-1；（4）牛磺酸＋羟自由基组：牛磺酸30mmol.L^-1 OH-0.1mmol.L。观察心肌细胞存活率和形态学，流式细胞仪双标法检测细胞凋亡率。结果：（1）羟自由基组心肌细胞存活率降低，和对照组比较有显性差异（P＜0．05），牛磺酸＋羟自由基组细胞存活率较羟自由基组高（P＜0．05），（2）Annexin V /PI-细胞即凋亡细胞在羟自由基组有较高的发生率，明显高于其他各组（P＜0．05）；牛磺酸＋羟自由基组的细胞凋亡率显低于羟自由基组（P＜0．05），（3）羟自由基组凋亡心肌细胞呈特征性超微结构。结论：牛磺酸能减轻外源性羟自由基诱导的心肌细胞凋亡。     

Peroxynitrite induced decrease in Na^＋, K^＋-ATPase activity is restored by taurine

AIM: Peroxynitrite (ONOO-) is a powerful oxidant shown to damage membranes. In the present study, the effect of taurine on changes of liver plasma membrane Na+, K+-ATPase induced by ONOO- was investigated. METHODS: Liver plasma membrane was exposed to ONOO-with or without taurine. Na+, K+-ATPase activity and lipid peroxidation as thiobarbituric acid reactive substances (TBARS) levels were measured. RESULTS: Different concentrations of ONOO- (100, 200, 500, and 1 000 μmol/L) were found to decrease liver plasma membrane Na+, K+-ATPase activity significantly. The depletion of enzyme activity was not concentration dependent. Effects of different concentrations of taurine on liver plasma membrane Na+, K+-ATPase activity were also measured. Taurine did not cause any increase in enzyme activity. When plasma membranes were treated with 200 μmol/L ONOO- with different concentrations of taurine, a restoring effect of taurine on enzyme activity was observed. TBARS levels were also measured and taurine was found to decrease the elevated values. CONCLUSION: Taurine is observed to act as an antioxidant of ONOO- to decrease lipid peroxidation and thus affect liver plasma membrane Na+, K+-ATPase by restoring its activity.     

Taurine improves neuron injuries and cognitive impairment in a mouse Parkinson’s disease model through inhibition of microglial activation

Clinical and experimental findings support the view that activation of hippocampus microglia through NADPH oxidase contributes to cognitive impairment in Parkinson's disease (PD). Taurine, an antioxidant, displays an exclusive physical property on brain function, such as learning and memory. To date, the role of taurine in improving cognitive impairment in PD is not fully uncovered. Hence, we evaluated the protective effect of taurine on cognitive ability and explored the related mechanism in the model built by paraquat and maneb (P + M)-induced PD mice. Then the ability of learning and memory was observed by Morris water maze, neuron loss was evaluated by immunohistochemistry in hippocampus, the level of postsynaptic density 95 (PSD95) and microglia activation was assessed by immunostaining, the molecules (gp91^phox, p47^phox, mac1, p-Src/Src and p-Erk/Erk) were examined by western blot. The results showed that taurine could alleviate the impairments in learning and memory induced by P + M injection in mice (decreased escape latency on day 4, P < 0.01; decreased swimming distance on day 4, P < 0.05; increased percent time in target quadrant, P < 0.05), corresponding with activation of microglia (decreased IBa-1 density, P < 0.001; decreased the protein expression of p47^phox, P < 0.05; decreased protein expression of gp91^phox, P < 0.01; decreased p-Src/Src, P < 0.01; decreased p-Erk/Erk, P < 0.01; decreased mac 1, P < 0.01), decreased neuron loss (increased number of NeurN⁺ neuron, P < 0.001; increased protein expression of NeruN, P < 0.01; decreased protein expression of caspase 3, P < 0.01) and increased PSD95 level in hippocampus (P < 0.01). The results indicated that mac1 and Src-Erk signaling was involved in increased NADPH oxidase expression in hippocampus microglia of P + M mice, and taurine could improve injuries in learning and memory through mac1 reduction. The new findings in mac1 triggering hippocampal microglia NADPH oxidase through Src/Erk pathway of the present study might provide a therapy target for PD.     

牛磺酸对海藻氨酸致痫大鼠海马谷氨酸转运体功能的影响

目的　研究海藻氨酸 (KA )致痫后海马神经元谷氨酸转运体 (Glu Ts)的功能变化 ,观察牛磺酸(Tau)对 KA点燃及点燃后海马神经元 Glu Ts功能的影响。方法　将 4 0只 Wistar大鼠随机分为对照组 ( 组 )、KA组 ( 组 )、Tau低剂量组 ( 组 )、Tau高剂量组 ( 组 ) ,每组各 10只。 组和 组分别腹腔注射低剂量 (1g/kg)和高剂量 (2 g/ kg) Tau,每日 1次 ,第 3天注射后 0 .5小时 ,与 KA组一起腹腔注射 KA10 mg/ kg,对照组腹腔注射生理盐水 (NS) 1m l。观察各组的痫性发作情况 ,并于 2 4小时后将大鼠处死 ,剥离右侧海马 ,制备海马突触颗粒 ,测定其摄取 3H- L -谷氨酸的功能。结果　与对照组相比 ,KA组点燃后海马神经元 Glu Ts功能降低 (P<0 .0 1) ;与KA组相比 , 、 组的点燃潜伏期延长 ,点燃率、痫性发作分级及死亡率均降低 ,海马神经元 Glu Ts功能增强 ,其作用与剂量呈正相关。结论　 KA可造成海马神经元 Glu Ts功能降低 ,Tau可抑制 KA引起的癫痫发作 ,其原因可能部分与改善海马神经元 Glu Ts功能有关。     

Amino acid signatures in the developing mouse retina

This study characterizes the developmental patterns of seven key amino acids: glutamate, γ-amino-butyric acid (GABA), glycine, glutamine, aspartate, alanine and taurine in the mouse retina. We analyze amino acids in specific bipolar, amacrine and ganglion cell sub-populations (i.e. GABAergic vs. glycinergic amacrine cells) and anatomically distinct regions of photoreceptors and Müller cells (i.e. cell bodies vs. endfeet) by extracting data from previously described pattern recognition analysis. Pattern recognition statistically classifies all cells in the retina based on their neurochemical profile and surpasses the previous limitations of anatomical and morphological identification of cells in the immature retina. We found that the GABA and glycine cellular content reached adult-like levels in most neurons before glutamate. The metabolic amino acids glutamine, aspartate and alanine also reached maturity in most retinal cells before eye opening. When the overall amino acid profiles were considered for each cell group, ganglion cells and GABAergic amacrine cells matured first, followed by glycinergic amacrine cells and finally bipolar cells. Photoreceptor cell bodies reached adult-like amino acid profiles at P7 whilst Müller cells acquired typical amino acid profiles in their cell bodies at P7 and in their endfeet by P14. We further compared the amino acid profiles of the C57Bl/6J mouse with the transgenic X-inactivation mouse carrying the lacZ gene on the X chromosome and validated this animal model for the study of normal retinal development. This study provides valuable insight into normal retinal neurochemical maturation and metabolism and benchmark amino acid values for comparison with retinal disease, particularly those which occur during development.     

Taurine reverses endosulfan-induced oxidative stress and apoptosis in adult rat testis

The present study was aimed to investigate the mechanistic aspect of endosulfan toxicity and its protection by taurine in rat testes. Pre-treatment with taurine (100 mg/kg/day) significantly reversed the decrease in testes weight, and the reduction in sperm count, motility, viability and daily sperm production in endosulfan (5 mg/kg/day)-treated rats. Sperm chromatin integrity and epididymal L-carnitine were markedly decreased by endosulfan treatment. Endosulfan significantly decreased the level of serum testosterone and testicular 3β-HSD, 17β-HSD, G6PDH and LDH-X. Sperm Δψm and mitochondrial cytochrome c content were significantly decreased after endosulfan. Testicular caspases-3, -8 and -9 activities were significantly increased but taurine showed significant protection from endosulfan-induced apoptosis. Oxidative stress was induced by endosulfan treatment as evidenced by increased H₂O₂ level and LPO and decreased the antioxidant enzymes SOD, CAT and GPx activities and GSH content. These alterations were effectively prevented by taurine pre-treatment.In conclusion, endosulfan decreases rat testes weight, and inhibits spermatogenesis and steroidogenesis. It induces oxidative stress and apoptosis by possible mechanisms of both mitochondria and non-mitochondria pathways. These data provide insight into the mode of action of endosulfan-induced toxicity and the beneficial role provided by taurine to counteract endosulfan-induced oxidative stress and apoptosis in rat testis.