牛磺酸对大鼠酒精性脑损伤组织中TNF-α水平的影响

目的观察牛磺酸对大鼠酒精性脑损伤组织中TNF-α水平的影响。方法采用给予乙醇灌胃制造酒精性脑损伤模型的方法,40只雄性Wistar大鼠随机分为对照组和牛磺酸组两组。对照组仅给予500ml/L的乙醇灌胃8周,牛磺酸组给予同等量乙醇灌胃,同时给予牛磺酸8周。研究结束后,抽取大鼠腹主动脉血液,断头取脑,检测各组血浆及脑组织中内皮素（ET）、肿瘤坏死因子（TNF-α）的水平。结果牛磺酸组血浆ET（[168.59±3.08）pg/mlvs（200.57±4.42）pg/ml]、脑组织匀浆TNF-α（[12.03±0.26）ng/gvs（19.06±0.31）ng/g]均明显低于对照组（P〈0.01）。结论牛磺酸可降低大鼠酒精性脑损伤组织中TNF-α水平。     

牛磺酸对沙土鼠短暂性前脑缺血作用研究

目的 观察牛磺酸对沙土鼠短暂性前脑缺血的保护作用。方法 结扎沙土鼠双侧颈动脉建立前脑缺血模型,缺血5 min后进行再灌注。在缺血1 h后经静脉给予2.5 mg/kg、5 mg/kg、15 mg/kg及50 mg/kg牛磺酸。再灌注7 d时,对沙土鼠的神经功能行为缺损进行评分,并留取全脑,观察海马CA1区锥体细胞的死亡情况。结果 2.5 mg/kg牛磺酸虽然改善前脑缺血5 min再灌注7 d时沙土鼠的行为,降低海马CA1区锥体细胞的死亡,但与缺血对照组相比,无统计学意义,5 mg/kg、15 mg/kg及50 mg/kg牛磺酸可明显改善前脑缺血沙土鼠的行为缺损（P分别为0.001、0.006和0.037）,降低海马CA1区锥体细胞的死亡（P均＜0.001）,其中,5 mg/kg、15 mg/kg和50 mg/kg牛磺酸组的锥体细胞的死亡低于2.5 mg/kg牛磺酸组（P分别为0.001、0.001和0.005）。结论 牛磺酸能以剂量依赖方式降低沙土鼠前脑缺血损伤,提示牛磺酸可能是一种有效的短暂性缺血的大脑保护剂。     

Antioxidants do not prevent acrylonitrile-induced toxicity

Several reports have recently described that acrylonitrile (ACN) toxicity resides in its capacity for inducing oxidative stress. ACN can be conjugated with glutathione (GSH), diminishing its cellular content, or being metabolized to cyanide. In the present report, we determine the effect of ACN on the viability of primary-cultured astrocytes as well as the oxidative damage generated by ACN by measuring GSH levels in primary cultured astrocytes. We also analyzed whether the ACN (2.5mM) toxicity could be avoided by using antioxidants such as taurine (5mM), N-acetylcysteine (20 mM), trolox (100 microM), estradiol (10 microM) and melatonin (100 nM-1mM). In this cell culture model, antioxidants were not able to prevent ACN-induced cell damage, with the exception of NAC, confirming that only GSH seems to play a key role in ACN-derived toxicity. Additionally, we measured different parameters of oxidative stress such as catalase activity, lipid peroxidation and GSH concentration, as indicators of the potential oxidative stress mediated by the toxicity of ACN, after exposure of Wistar rats to a concentration of 200 ppm ACN for 14 days. At the concentration assayed, we did not find any evidence of oxidative damage in the brain of ACN-treated rats.     

牛磺酸对酒精性脂肪肝抗氧化作用的研究

[目的]研究牛磺酸对酒精性脂肪肝动物模型的抗氧化效果。[方法]将小鼠随机分为3组,包括正常对照组、酒精性脂肪肝模型组、牛磺酸干预组。2周后分别检测肝脏中脂褐质LF、血清MDA、SOD以及GSH-PX等血生化指标,并对小鼠肝脏进行病理及免疫组化量化分析。[结果]牛磺酸能显著降低小鼠血清MDA和肝脏中脂褐质LF的含量,并增强血清中SOD以及GSH-PX的活性;肝脏免疫组化量化分析显示,牛磺酸可显著改善酒精对小鼠肝脏的损伤。[结论]牛磺酸可能通过抗氧化的途径来减轻酒精对肝脏导致的损伤。     

Neurites outgrowth and amino acids levels in goldfish retina under hypo-osmotic or hyper-osmotic conditions

Amino acids are known to play relevant roles as osmolytes in various tissues, including the retina. Taurine is one of these active molecules. In addition, taurine stimulates outgrowth from the goldfish retina by mechanisms that include extracellular matrix, calcium fluxes and protein phosphorylation. The present report aims to explore the effect of medium osmolarity on goldfish retinal outgrowth and the possible modifications produced by changing eye osmolarity on amino acid levels in the retina. Goldfish retinal explants were obtained 10 days after crush of the optic nerve and cultured under iso-, hypo- or hyper-osmotic conditions. Hypo-osmotic medium was prepared by diluting the solutions 10% twice, preserving fetal calf serum concentration. Hyper-osmotic medium was done by adding 50 or 100 mM urea or mannitol. Evaluation of length and density of neurites was performed 5 days after plating. Outgrowth was reduced in hypo- and in hyper-osmotic conditions. Taurine, 4 mM, increased length and density of neurites in iso-osmotic, and produced stimulatory effects under both hyper-osmotic conditions. The in vivo modification of osmolarity by intraocular injection of water or 100 mM urea modified levels of free amino acids in the retina. Taurine and aspartate retinal levels increased in a time-dependent manner after hypo- and hyper-osmotic solution injections. Serine, threonine, arginine, γ-aminobutyric acid, alanine and tyrosine were elevated in hyper-osmotic conditions. Outgrowth in vitro, after in vivo osmolarity changes, was higher in the absence of taurine, but did not increase in the presence of the amino acid. The fact that certain outgrowth took place in these conditions support that the impairment was not due to tissue damage. Rather, the effects might be related to the cascade of kinase events described during osmolarity variations. The time course under these conditions produced adjustments in ganglion cells probably related to taurine transporter, and phosphorylation of specific proteins.     

Attenuation of tamoxifen-induced hepatotoxicity by taurine in mice

BACKGROUND: One of the most attractive approaches to disease prevention involves the use of natural antioxidants to protect tissue against toxic injury. We investigated the modulatory effects of exogenously administered taurine on the toxicity of the anticancer drug tamoxifen with special reference to protection against disruption of drug metabolizing and antioxidant enzymes in Swiss albino mice. METHODS: Male Swiss albino mice were divided into 4 groups. The extent of lipid peroxidation was evaluated in terms of thiobarbituric acid reactive substances formed. The following assays were performed in the hepatic tissue (a) antioxidant enzymes such as superoxide dismutase and catalase, (b) cytochrome P450 content, (c) glutathione-metabolizing enzymes such as glutathione peroxidase, glutathione reductase, glutathione-S-transferase and glucose 6-phosphate dehydrogenase, and (d) low molecular weight antioxidants (reduced glutathione, ascorbic acid) and protein carbonyl content. RESULTS: Tamoxifen induced lipid peroxidation, protein carbonyl content and inhibited the enzymes of antioxidant defense system. It was also observed that the activities of antioxidant enzymes and glutathione-metabolizing enzymes were considerably stabilized in mice pretreated with taurine. CONCLUSION: Taurine protects the integrity of the hepatic tissue by stabilizing the reactive oxygen species mediated lipid peroxidation and protein carbonyl formation. Additionally taurine may prove to be efficacious as an antioxidant in tamoxifen-induced hepatotoxicity.     

应用高效液相色谱法测定母乳化奶粉中的牛磺酸

牛磺酸作为新型营养强化剂添加在第二代母乳化奶粉中。作者应用高效液相色谱法对母乳化奶粉中的牛磺酸进行定量分析，样品经1％偏磷酸提取→钠柱分离→柱后OPA衍生→荧光检测器检测定量。操作简便、快速，提取完全，牛磺酸出峰时间8．738min，回收率99．5％，变异系数2．19％，最低检出量20ng，为一个较理想的定量方法。     

Taurine induces upregulation of p53 and Beclin1 and has antitumor effect in human nasopharyngeal carcinoma cells in vitro and in vivo

Taurine is an amino acid that has several physiological functions. Previously, we reported the apoptosis-inducing effect of taurine in human nasopharyngeal carcinoma (NPC) cells in vitro. However, the effect of taurine on NPC cell growth in vivo has not been elucidated. Autophagy plays an important role in cell metabolism and exhibits antitumor effects under certain conditions. In this study, we investigated the effects of taurine on apoptosis- and autophagy-related molecules in NPC cells in vitro and in vivo. In our in vitro study, NPC cells (HK1-EBV) were treated with taurine, and Western blot and immunocytochemical analyses revealed that taurine co-upregulated Beclin 1 and p53, with autophagy upregulation. In the in vivo study, we used a nude mouse model with subcutaneous xenografts of HK1-EBV cells. Once the tumors reached 2–3 mm in diameter, the mice were provided with distilled water (control group) or taurine dissolved in distilled water (taurine-treated group) ad libitum (day 1) and sacrificed on day 13. The volume and weight of the tumors were significantly lower in the taurine-treated group. Using immunohistochemistry (IHC), we confirmed that taurine treatment reduced the distinct cancer nest areas. IHC analyses also revealed that taurine promoted apoptosis, as evidenced by an increase in cleaved caspase-3, accompanied by upregulation of p53. Additionally, taurine increased LC3B and Beclin 1 expression, which are typical autophagy markers. The present study demonstrated taurine-mediated tumor growth suppression. Therefore, taurine may be a novel preventive strategy for NPC.