牛磺酸对高血压和血管活性物质的影响

在原发性高血压(EH)患者、大鼠腹主动脉狭窄和高盐摄入引起高血压模型上,观察到口服牛磺酸治疗4周后均明显降低平均动脉压和收缩压,42.2%的患者血压恢复正常,并能抑制EH患者和高血压大鼠血浆内皮素(ET)、血管紧张素II(AII)水平的升高,增加高血压大鼠血浆降钙素基因相关肽(CGRP)和主动脉组织中的牛磺酸含量.以上结果表明,牛磺酸在降压作用同时伴有缩血管物质的降低和舒血管物质的增加,为以牛磺酸作为降血压辅助药物提供了依据.     

Sodium-taurine cotransport in reptilian renal brush-border membrane vesicles

The coupled transport of Na⁺ with taurine into snake renal brush-border membrane vesicles (BBMV) was studied using 5-s uptake conditions. Taurine transport into snake renal BBMV involved two parallel processes, one saturable (Na⁺-dependent) and one (Na⁺-independent) that behaved like passive diffusion. Below 1 mM taurine concentration, the Na⁺-dependent system accounted for 60% of total taurine uptake. Over both low (0.001–0.80 mM) and high (0.8–5.0 mM) taurine concentration ranges, the Na⁺-dependent taurine uptake within each range showed Michaelis-Menten kinetics, suggesting the presence of two independent saturable Na⁺-dependent transport systems for taurine. The high-affinity, low-capacity system saturated above 100 M with a K _m of 71.4±45.7 M and a maximum velocity (V _max) of 21.9±3.77 pmol (mg protein)^–1 (5 s)^–1. The low-affinity, high-capacity system saturated above 1 mM, with a K _m of 1.11±0.63 mM and a V _max of 252±47 pmol (mg protein)^–1 (5 s)^–1. The stoichiometric relationship between external Na⁺ concentration and taurine uptake (at 10 M) by the high-affinity BBMV transport system was examined by the activation method under short-circuited conditions. The 5-s rate of taurine transport was a sigmoid function of increasing extravesicular Na⁺ concentration. Kinetic analysis of the interaction of Na⁺ with the high-affinity taurine transport system suggested that 3 Na⁺ ions (3.2±0.7) may be involved with 1 taurine molecule in the transport event. The data suggest the presence of a highly efficient and high-affinity reabsorptive taurine transport system on the luminal membrane of the kidney of the garter snake, a species that can secrete taurine in vivo.     

Some neurochemical studies on auditory regions of mouse brain

Summary The mouse brain auditory pathway has been dissected into five regions: geniculate bodies, posterior colliculi, superior olives, cochlear nuclei, and cochleas. The following analyses were made in these regions and in the auditory cortex: protein, glutamate, -aminobutyrate, taurine, choline acetyltransferase, and glutamate decarboxylase.Taurine levels (nmol · mg of protein^-1) were highest in cortex (93) and geniculate bodies (60) and lowest in the cochlear nuclei (27) and cochleas (29).Concentrations of -aminobutyrate (same units) were highest in the geniculate bodies (28), low in the superior olives and cochlear nuclei (9 to 10), and undetectable in the cochleas. The distribution of glutamate decarboxylase activity reflected that of -aminobutyrate.The activities of choline acetyltransferase (nmol · of acetylcholine synthesized · h · ^-1 mg of protein^-1) were highest in the superior olives (60) and low in the cochleas (3).These results are interpreted as biochemical support for previous physiological and pharmacological identification of the olivo-cochlear bundle as cholinergic and the cochlear-nucleus neurones as non-cholinergic. The results also provide further evidence for a role of GABA in the posterior colliculi, but not in the cochleas.     

Can energy drinks reduce the depressor effect of ethanol? An experimental study in mice

Although the popularization of the combined use of alcoholic beverages and energy drinks (ED) containing caffeine, taurine and other substances has increased, there are no controlled experimental studies on the effects of ED alone or combined with ethanol. This work aimed at evaluating the effects of different doses of ED combined or not with ethanol, on the locomotor activity of Swiss mice. The administration of 3.57, 10.71 or 17.86 ml/kg of ED alone increased the locomotor activity of the animals in relation to a control group. Low doses of ethanol (0.5, 1.0 and 1.5 g/kg) alone or in combination with 10.71 ml/kg of ED did not affect their locomotor activity. However, the reduction of activity observed after 2.5 g/kg of ethanol was antagonized by 10.71 ml/kg of ED. Further studies on the mechanisms of this interaction are still needed.     

IL-1β、TNF-α和IFN-γ引起的大鼠胰岛细胞凋亡及牛磺酸的影响

目的： 观察白细胞介素-1β(IL-1β)、肿瘤坏死因子-α（TNF-α）和γ-干扰素（IFN-γ）引起胰岛细胞凋亡、胰岛素分泌、Bcl-xL和Bax蛋白表达变化及其牛磺酸的影响。方法： 应用体外单层培养Wistar大鼠胰岛细胞，分别检测IL-1β、TNF-α和 IFN-γ对胰岛细胞凋亡细胞百分率、DNA片段、培养液中NO^-₂/ NO^-₃含量及NOS活性、胰岛素分泌、Bcl-xL和Bax表达的影响，并进一步观察牛磺酸的作用。结果： IL-1β、TNF-α和 IFN-γ联合可诱导胰岛细胞凋亡率明显增加，DNA明显片段化，同时NO^-₂/ NO^-₃含量和NOS活性亦明显升高，胰岛素分泌明显降低, Bcl-xL表达下降和Bax表达增强（P<0.01）；牛磺酸能阻断上述细胞因子的作用（P<0.01），并有一定的剂量依赖性。结论：牛磺酸能够改善IL-1β、TNF-α和 IFN-γ诱导的胰岛细胞凋亡，其机制可能与抑制NOS活性从而减少NO的生成以及下调Bax/Bcl-xL比例有关。     

牛磺酸对大鼠肢体缺血再灌注后肺损伤时细胞凋亡的影响

目的:从细胞凋亡的角度探讨肢体缺血再灌注(LIR)后急性肺损伤(ALI)的发病机制及牛磺酸的影响。方法:复制大鼠肢体缺血再灌注(LIR)损伤动物模型,采用TUNEL法、电泳法、半定量逆转录聚合酶链反应(SqRT-PCR)及免疫组织化学等技术观察LIR后肺损伤发生过程中,肺泡上皮及血管内皮细胞凋亡变化以及Fas/FasL系统蛋白质和mRNA表达的改变。结果:大鼠LIR后,肺泡上皮细胞和肺血管内皮细胞凋亡明显增加;肺组织Fas/FasLmRNA和蛋白质表达明显上调,DNA断链率、组织钙含量和活性氧(ROS)升高,且与肺泡上皮及血管内皮细胞凋亡的增加相一致。结论:肺泡上皮及血管内皮细胞凋亡以及Fas/FasL系统表达明显上调可能参与LIR后ALI的发生;牛磺酸可减少肺组织细胞凋亡,但并非通过影响Fas/FasL基因表达而实现其保护效应。     

Is there a role of taurine bromamine in inflammation? Interactive effects with nitrite and hydrogen peroxide

Objective and Design: The myeloperoxidase system of neutrophils generates chlorinating and brominating oxidants in vivo. The major haloamines of the system are taurine chloramine (TauCl) and taurine bromamine (TauBr). It has been demonstrated in vitro that TauCl exerts both antiinflammatory and anti-bacterial properties. Much less is known about TauBr. The present study was conducted to compare bactericidal and immunoregulatory capacity of TauBr with that of the major chlorinating oxidants: HOCl and TauCl. Moreover, the effect of nitrites and H₂O₂ on TauBr activity was investigated.Materials: TauBr was prepared by reaction of HOBr with taurine. The reaction was monitored by UV absorption spectra.Methods: Bactericidal activity of TauBr, TauCl and HOCl was tested by incubation of E. coli with the compounds and determined by the pour-plate method. To test the anti-inflammatory activity the compounds were incubated with LPS and IFN- stimulated murine peritoneal macrophages. The production of following mediators was measured: nitrites by Griess reaction; TNF-, IL-6, IL-10, IL-12p40 using capture ELISA. In some experiments the compounds were incubated with either nitrites or H₂O₂.Results: In our experimental set-up TauBr and HOCl exerted strong bactericidal effects on E. coli (MBC = 110 M and 8 M, respectively), while TauCl (< 1000 M) did not kill test bacteria. However, both, TauBr and TauCl, at noncytotoxic concentrations (< 300 M) inhibited the cytokine and nitric oxide production by macrophages. H₂O₂ completely abolished the biological activities of TauBr but not those of TauCl. Nitrites did not affect any activity of TauBr or TauCl while they diminished the HOCl^– mediated bacterial killing.Conclusion: TauBr, despite very low concentration of Br^– in body fluids, may support TauCl and HOCl in the regulation of inflammatory response and in killing of bacteria by neutrophils. However, TauBr activity in vivo will depend on the presence of H₂O₂ and possible other mediators of inflammation which can compete with target molecules for TauBr.Received 16 August 2004; returned for revision 16 September 2004; accepted by A. Falus 13 October 2004     

Efficacy of a 'functional energy drink' in counteracting driver sleepiness

Driver sleepiness is a major cause of serious road crashes. Coffee is often used as an effective countermeasure to driver sleepiness. However, the caffeine levels in coffee are variable, whereas certain proprietary "functional energy drinks" (FEDs) contain known levels of caffeine (and other ingredients). We investigated the effectiveness of a well-known FED in reducing sleepiness in drivers. Twelve healthy young adults drove an instrumented car simulator between 14:00 and 17:00 h. Their sleepiness was enhanced by sleep restriction to 5 h the night before. Following a pretreatment 30-min drive and at the beginning of a 30-min break, participants were given double-blind 250-ml FED (containing sucrose, glucose, 80-mg caffeine, taurine, glucuronolactone and vitamins) vs. a control drink with the same volume and same taste but without caffeine, taurine and glucuronolactone. Two hours of continuous driving ensued. Lane drifting, subjective sleepiness and the electroencephalogram (EEG) were monitored throughout. Compared with the control, the FED significantly reduced sleep-related driving incidents and subjective sleepiness for the first 90 min of the drive. There was a trend for the EEG to reflect less sleepiness during this period. It was concluded that the FED is beneficial in reducing sleepiness and sleep-related driving incidents under conditions of afternoon monotonous driving following sleep restriction the night before.     

牛磺酸对培养乳鼠心肌细胞缺氧坏死的保护作用

目的　观察牛磺酸 (Tau)对缺氧引起的心肌细胞坏死有无直接保护作用。方法　将培养心肌细胞分为正常对照、Tau对照缺氧 Tau和缺氧 4个组。测定培养细胞上清液中肌酸磷酸激酶 (CPK)活性 ,用原子吸收法测定细胞内钙、镁含量 ,Annexin V- FITC/ PI双染流式细胞术和台盼蓝染色镜检检测坏死细胞。结果　 Tau可使缺氧时培养细胞上清液中CPK活性降低 30 % ,坏死细胞减少大约 2 0 %。减少细胞内钙超载和镁丢失。结论　 Tau对缺氧导致的心肌细胞坏死有直接保护作用 ,此作用可能与减少细胞内钙超载和镁丢失有关。