Taurine: a promising nutraceutic in the prevention of retinal degeneration

Taurine is considered a non-essential amino acid because it is synthesized by most mammals.However,dietary intake of taurine may be necessary to achieve the physiological levels required for the development,maintenance,and function of certain tissues.Taurine may be especially important for the retina.The concentration of taurine in the retina is higher than that in any other tissue in the body and taurine deficiency causes retinal oxidative stress,apoptosis,and degeneration of photoreceptors and retinal ganglion cells.Low plasma taurine levels may also underlie retinal degeneration in humans and therefore,taurine administration could exert retinal neuroprotective effects.Taurine has antioxidant,anti-apoptotic,immunomodulatory,and calcium homeostasis-regulatory properties.This review summarizes the role of taurine in retinal health and disease,where it appears that taurine may be a promising nutraceutical.

Taurine attenuates activation of hepatic stellate cells by inhibiting autophagy and inducing ferroptosis

BACKGROUND Liver fibrosis is a compensatory response during the tissue repair process in chronic liver injury,and finally leads to liver cirrhosis or even hepatocellular carcinoma.The pathogenesis of hepatic fibrosis is associated with the progressive accumulation of activated hepatic stellate cells(HSCs),which can transdiffer-entiate into myofibroblasts to produce an excess of the extracellular matrix(ECM).Myofibroblasts are the main source of the excessive ECM responsible for hepatic fibrosis.Therefore,activated hepatic stellate cells(aHSCs),the principal ECM producing cells in the injured liver,are a promising therapeutic target for the treatment of hepatic fibrosis.AIM To explore the effect of taurine on aHSC proliferation and the mechanisms involved.METHODS Human HSCs(LX-2)were randomly divided into five groups:Normal control group,platelet-derived growth factor-BB(PDGF-BB)(20 ng/mL)treated group,mmol/L,respectively)with PDGF-BB(20 ng/mL)treated group.Cell Counting Kit-8 method was performed to evaluate the effect of taurine on the viability of aHSCs.Enzyme-linked immunosorbent assay was used to estimate the effect of taurine on the levels of reactive oxygen species(ROS),malondialdehyde,glutathione,and iron concen-tration.Transmission electron microscopy was applied to observe the effect of taurine on the autophagosomes and ferroptosis features in aHSCs.Quantitative real-time polymerase chain reaction and Western blot analysis were performed to detect the effect of taurine on the expression ofα-SMA,Collagen I,Fibronectin 1,LC3B,ATG5,Beclin 1,PTGS2,SLC7A11,and p62.RESULTS Taurine promoted the death of aHSCs and reduced the deposition of the ECM.Treatment with taurine could alleviate autophagy in HSCs to inhibit their activation,by decreasing autophagosome formation,downregulating LC3B and Beclin 1 protein expression,and upregulating p62 protein expression.Meanwhile,treatment with taurine triggered ferroptosis and ferritinophagy to eliminate aHSCs characterized by iron overload,lipid ROS accumu-lation,glutathione depletion,and lipid peroxidation.Furthermore,bioinformatics analysis demonstrated that taurine had a direct targeting effect on nuclear receptor coactivator 4,exhibiting the best average binding affinity of-20.99 kcal/mol.CONCLUSION Taurine exerts therapeutic effects on liver fibrosis via mechanisms that involve inhibition of autophagy and trigger of ferroptosis and ferritinophagy in HSCs to eliminate aHSCs.

Emergence of taurine as a therapeutic agent for neurological disorders

Taurine is a sulfur-containing,semi-essential amino acid that occurs naturally in the body.It alternates between inflammation and oxidative stress-mediated injury in various disease models.As part of its limiting functions,taurine also modulates endoplasmic reticulum stress,Ca^(2+)homeostasis,and neuronal activity at the molecular level.Taurine effectively protects against a number of neurological disorders,including stro ke,epilepsy,cerebral ischemia,memory dysfunction,and spinal cord injury.Although various therapies are available,effective management of these disorders remains a global challenge.Approximately 30 million people are affected worldwide.The design of taurine fo rmation co uld lead to potential drugs/supplements for the health maintenance and treatment of central nervous system disorders.The general neuroprotective effects of taurine and the various possible underlying mechanisms are discussed in this review.This article is a good resource for understanding the general effects of taurine on various diseases.Given the strong evidence for the neuropharmacological efficacy of taurine in various experimental paradigms,it is concluded that this molecule should be considered and further investigated as a potential candidate for neurotherapeutics,with emphasis on mechanism and clinical studies to determine efficacy.

Mitigating diabetes-related complications:Empowering metformin with cholecalciferol and taurine supplementation in type 2 diabetic rats

BACKGROUND Type 2 diabetes is one of the most prevalent chronic diseases worldwide,significantly impacting patients'quality of life.Current treatment options like metformin(MET)effectively counteract hyperglycemia but fail to alleviate diabetes-associated complications such as retinopathy,neuropathy,nephropathy,hepatopathy,and cardiovascular diseases.AIM To propose the supplementation of cholecalciferol(CHO)and taurine(TAU)to enhance MET efficacy in controlling diabetes while minimizing the risk of associated complications.METHODS The study involved sixty rats,including ten non-diabetic control rats and fifty experimental rats with type 2 diabetes induced by streptozotocin.The experimental rats were further subdivided into positive control and treatment subgroups.The four treatment groups were randomly allocated to a single MET treatment or MET combined with supplements either CHO,TAU,or both.RESULTS Diabetic rats exhibited elevated levels of glucose,insulin,Homeostasis Model Assessment of Insulin Resistance(HOMA-IR),glycated hemoglobin percentage,lipid markers,aspartate aminotransferase,and malondialdehyde,along with reduced levels of antioxidant enzymes(catalase and superoxide dismutase).The administration of CHO and TAU supplements alongside MET in diabetic rats led to a noticeable recovery of islet mass.The antioxidative,anti-inflammatory,and anti-apoptotic properties of the proposed combination therapy significantly ameliorated the aforementioned abnormalities.CONCLUSION The supplementation of CHO and TAU with MET showed the potential to significantly improve metabolic parameters and protect against diabetic complications through its antioxidative,anti-inflammatory,and antiapoptotic effects.

Encapsulating taurine into liposomes:A promising therapeutic for liver fibrosis

We summarize the mechanism by which taurine(Tau)inhibits autophagy and induces iron apoptosis in hepatic stellate cells.Tau interacts with autophagy regulates multifunctional proteins,microtubule-associated protein 1 light chain 3 Beta,and autophagy-related gene 5 to inhibit autophagy,binds to ferritin heavy chain 1 and nuclear receptor coactivator 4 to trigger ferritin autophagy,and interacts with glutathione peroxidase 4 to promote iron apoptosis.There is a solid rationale for developing Tau-based therapies targeting autophagy and ferroptosis regulation.From a pharmaceutical point of view,there are certain requirements for Tau protein delivery systems,such as loading efficiency,stability,and targeting.Nanomaterials should also contain a hydrophilic motif similar to Tau to optimize loading efficiency.Since Tau is a hydrophilic molecule with high water solubility,liposomes,micelles,and amphiphilic polymer nanoparticles may represent a superior choice.The nanostructure of the liposome includes a water region and a lipid membrane to sequester hydrophilic and hydrophobic drugs,respectively,whereas Tau is expected to be loaded into the water region.In addition,a representative method of actively targeting hematopoietic stem cells is introduced.A Tau-based method for the treatment of liver fibrosis is proposed based on the formulation of common liposomes(lecithin plus cholesterol).

Effects of Taurine on Physiological Properties of Lyium bararum L. Seedlings

[Objective] The study was to investigate the relationship between taurine and physiological activities of Lyium bararum seedlings. [Method] Through applying different concentrations of taurine(0, 10, 100, 500, 1 000, 5 000 mg/L), the photosynthetic rate(Pn), stomatal conductance(Gs), and the activities of membrane protective enzymes superoxide dismutase(SOD) and peroxidase (POD) in the treated L. bararum seedlings were measured. [Result] Treatment of proper taurine concentration could to some extent enhance Pn and increase the POD and SOD activities, and meanwhile decreased the Gs and MDA content. And the optimum application amount of taurine was determined to be 500 mg/L. [Conclusion] Proper concentration of taurine has protective effects on the cell membrane of L. bararum seedlings.

Effect of taurine on GFAP and TauT expressions in rat retinal Müller cells in high glucose culture

Objective： To detect the expression of glial fibrillary acid protein （GFAP） and taurine transporter （TauT） in the retinal Müller cells in high glucose culture with taurine and to explore the influence of glucose on the taurine transporting, and the possible protective effects of taurine on MUller cells in early diabetic retinopathy. Methods： The Müller cells from the rat retina were cultured in high glucose, and GFAP and Taut expressions were detected in the cells treated with different doses of taurine by immuocytochemical fluorescein staining and Western blotting. Results： High glucose enhanced the expression of GFAP and decreased the expression of TauT in Müller cells. Taurine decreased the up-regulation of GFAP in the cells which was induced by high glucose; 0. 1-10 mmol/L taurine increased the expression of TauT in Müller cells. Conclusion： Taurine can inhibit the changes in Müller cell resulted from high glucose.

Taurine牛基因组序列图:反刍动物生物学及其进化论的窗口

为了理解反刍动物的生物学和进化论,牛的基因组图被测定出有大约7倍区域(Genome sevenfold coverage)。整个序列含有最低限度22000个基因,有一套核心基因14345个,是7个哺乳动物种共享拥有的源祖同源基因或直系同源基因(Ortholog),其中有1217个基因在非真哺乳动物亚纲(有袋目动物或单孔目动物)基因组图中不存在或没被检测到。牛染色体特有的进化演变区的片断复制的密度较高,重复元素丰富,并且这种种类特有的基因变异与产乳和免疫反应有关。表达代谢的基因一般是高度保守的,但是人类跟它们同源的5个参与代谢的源祖同源基因已丢失或广泛地发生了漂移。牛的基因组图谱就这样为理解哺乳动物进化和加速家畜泌乳和产肉的遗传改进提供了一种资源。

Selective depression action of taurine in flotation separation of specularite and chlorite

Chlorite,as the most representative gangue mineral associated with specularite,of which the separation of these two minerals is difficult.This paper investigated the depression effect of taurine on specularite/chlorite separation via flotation experiments,adsorption tests,contact angle measurements,Zeta potential detection,FT-IR measurements,and XPS analyses.The results of single mineral flotation indicated that chlorite could be depressed selectively by taurine with the recovery of less than 30%,but the floatability of specularite remains high with recovery rate of 81.77%at pH 10.The artificial mixed mineral flotation results confirmed the effectiveness of taurine as a depressant.Surface adsorption,contact angle,and Zeta potential detection revealed taurine primarily adsorbs on the chlorite surface,which hampered the DDA’s subsequent adsorption and results in the chlorite’s poor floatability.The FT-IR spectra and XPS analyses provided further proof that taurine adsorbed on chlorite surface as an electron donor,and part of the electrons transferred from the sulfonic acid group of taurine to metal ions during the adsorption process.In addition,the hydrogen bond between amino-group of taurine and O ions in chlorite surface was also formed in the adsorption process.Finally,optimized adsorption configurations of taurine on chlorite surfaces were proposed.

Natural taurine promotes apoptosis of human hepatic stellate cells in proteomics analysis

AIM:To study the differential expression of proteins between natural taurine treated hepatic stellate cells and controls, and investigate the underlying regulatory mechanism of natural taurine in inhibiting hepatic fibrosis.METHODS: A proteomic strategy combining two-dimensional gel electrophoresis and ultraperform ance liquid chromatographyelectrospray ionizationtandem mass spectrometry (UPLCESIMS/MS) was used to study the differential expression of proteins and Western blotting was used to validate the results. Gene ontology (GO) method was utilized to analyze the functional enrichment of differentially expressed proteins. Flow cytometry was performed to compare the apoptosis rate between taurinetreated and untreated hepatic stellate cells (HSCs).RESULTS: Nineteen differentially expressed proteins (11 upregulated and 8 downregulated) were identifiedby 2D/MS, and the expression profiles of GLO1 and ANXA1 were validated by Western blotting. GO analysis found that these differentially expressed proteins were enriched within biological processes such as "cellular apoptosis", "oxidation reaction" and "metabolic process" in clusters. Flow cytometric analysis showed that taurinetreated HSCs had a significantly increased apoptosis rate when compared with the control group.CONCLUSION: Natural taurine can promote HSC apoptosis so as to inhibit hepatic fibrosis.

Determination of Taurine in Biological Samples by High-Performance Liquid Chromatography Using 4-Fluoro-7-Nitrobenzofurazan as a Derivatizing Agent

Objective A highly sensitive and rapid high‐performance liquid chromatography method with pre‐column derivatization with 4‐fluoro‐7‐nitrobenzofurazan was developed for determination of taurine in biological samples,including plasma,brain,and liver.Methods The optimum derivatization reaction temperature was 70℃,and at this temperature the reaction was complete within 3 min.The derivatized taurine was separated using phosphate buffer （0.02 mol/L,pH 6.0）：acetonitrile （84：16,v/v） as the mobile phase at a flow rate of 1.0 mL/min,and a column temperature of 25℃.The taurine derivatives were separated within 20 min （tR：14.5 min） and fluorometrically detected at 530 nm with excitation at 470 nm.Results The intra‐ and the inter‐day coefficients of variation for the method were 5.3% and 7.7%,respectively.The calibration curve was linear from 0.1 μmol/L to 30.0 μmol/L with a correlation coefficient of 0.9995.Conclusion This method can be used to determine the taurine contents in plasma,brain,and liver from normal rats and human plasma.

Antenatal taurine reduces cerebral cell apoptosis in fetal rats with intrauterine growth restriction

From pregnancy to parturition, Sprague-Dawley rats were daily administered a low protein diet to establish a model of intrauterine growth restriction. From the 12th day of pregnancy, 300 mg/kg taurine was daily added to food until spontaneous delivery occurred. Brain tissues from normal neonatal rats at 6 hours after delivery, neonatal rats with intrauterine growth restriction, and neo- natal rats with intrauterine growth restriction undergoing taurine supplement were obtained for fur- ther experiments. The terminal deoxyribonucleotidyl transferase （TdT）-mediated biotin-16-dUTP nick-end labeling assay revealed that the number of apoptotic cells in the brain tissue of neonatal rats with intrauterine growth restriction significantly increased. Taurine supplement in pregnant rats reduced cell apoptosis in brain tissue from neonatal rats with intrauterine growth restriction. Immu- nohistochemical staining revealed that taurine supplement increased glial cell line-derived neuro- trophic factor expression and decreased caspase-3 expression in the cerebral cortex of intrauterine growth-restricted fetal rats. These results indicate that taurine supplement reduces cell apoptosis through the glial cell line-derived neurotrophic factor-caspase-3 signaling pathway, resulting in a protective effect on the intrauterine growth-restricted fetal rat brain.

Attenuation of portal hypertension by natural taurine in rats with liver cirrhosis

AIM： To investigate the inhibitory effect of natural taurine （NTau） on portal hypertension （PHT） in rats with experimentally-induced liver cirrhosis （LC）. METHODS： Experimentally-induced LC Wistar rats （20 rats/group） were treated with either oral saline or oral NTau for 6 consecutive weeks. Evaluation parameters included portal venous pressure （PVP）, portal venous resistance （PVR）, portal venous flow （PVF）, splanchnic vascular resistance （SVR） and mean arterial pressure （NAP）. Vasoactive substance levels including nitric oxide （NO）, nitric oxide synthase （NOS） and cyclic guanosine monophosphate （cGMP） were also measured. Histological investigation of type Ⅰ and Ⅲ collagen （COL Ⅰ and Ⅲ） and transforming growth factor-β1 （TGF-β1） was also performed. RESULTS： Treatment with NTau （1） significantly decreased PVP, PVR and PVF, and increased MAP and SVP; （2） markedly increased the vascular compliance and reduced the zero-stress of the portal vein; （3） markedly decreased the amount of NO and cGMP and activity of NOS; and （4） improved the pathological status of the liver tissue and reduced the expression of COL Ⅰ, COL Ⅲ and TGF-β1. CONCLUSION： NTau inhibited the LC-induced PHT by improving hyperdynamic circulation, morphology of liver and biomechanical properties of the portal vein in experimentally-induced LC rats.

Study on the effect of doxorubicin on expressions of genes encoding myocardial sarcoplasmic reticulum Ca^2＋ transport proteins and the effect of taurine on myocardial protection in rabbits

To investigate the effect of doxorubicin(DOX) on gene expression of the myocardial sarcoplasmic reticulum (SR)Ca 2+ transport proteins and the mechanism of taurine(Tau) protecting cardiac muscle cells, 9 rabbits were injected with DOX , 8 rabbits with DOX and Tau, and 9 rabbits with normal saline. Cardiac function , concentration of calcium in cardiomyocytes (Myo[Ca 2+ ] \%i\%), activity of SR Ca 2+ ATPase(SERCA2a), level of SERCA2a mRNA and Ca 2+ released channels(RYR2)mRNA were detected. The left ventricle tissues were observed by electron microscopy. The results showed that cardiac index, left ventricular systolic pressure, activity of SR Ca 2+ ATPase and level of SERCA2a mRNA decreased , while Myo[Ca 2+ ] \%i\% increased in DOX treated rabbits. DOX could not affect the level of RYR2 mRNA. Tau intervention could alleviate the increase of left ventricular diastolic pressure, Myo[Ca 2+ ] \%i\% and the decrease of SERCA2a mRNA induced by doxorubicin. The results suggested that downregulation of SERCA2a gene expression was an important mechanism of DOX induced cardiomyopathy and that Tau could partially improve the heart function by reducing calcium overload and alleviating downregulation of SERCA2a mRNA.

Pegylated interferon-alpha plus taurine in treatment of rat liver fibrosis

AIM: To investigate the antif ibrotic effects of peginterferon- alpha 2b and taurine on oxidative stress markers and hepatocellular apoptosis. METHODS: Sixty rats with CCl4-induced liver fibrosis were divided into 4 groups (n = 15). Group 1 was left for spontaneous recovery (SR). Groups 2-4 received peginterferon-alpha 2b, taurine, and their combination, respectively, for four weeks. Histological f ibrosis scores, histomorphometric analysis, tissue hydroxyproline, tissue MDA, GPx and SOD activities were determined. Activated stellate cells and hepatocellular apoptosis were also evaluated. RESULTS: The degree of f ibrosis decreased in all treatment groups compared to spontaneous recovery group. Taurine alone and in combination with peginterferon-alpha 2b reduced oxidative stress markers, but peginterferon-alpha 2b alone did not. Apoptotic hepatocytes and activated stellate cells were higher in groups 2-4 than in group 1. Combined taurine and peginterferon-alpha 2b further reduced fibrosis and increased activated stellate cell apoptosis, but could not improve oxidative stress more than taurine alone.CONCLUSION: Peginterferon-alpha 2b exerts anti- f ibrotic effects on rat liver fibrosis. It seems ineffective against oxidative stress in vivo. Peginterferon-alpha 2b in combination with taurine seems to be an antif ibrotic strategy.

Integrated network analysis of transcriptomic and protein-protein interaction data in taurine-treated hepatic stellate cells

BACKGROUND Studies show that the antifibrotic mechanism of taurine may involve its inhibition of the activation and proliferation of hepatic stellate cells(HSCs). Since the molecular mechanism of taurine-mediated antifibrotic activity has not been fully unveiled and is little studied, it is imperative to use "omics" methods to systematically investigate the molecular mechanism by which taurine inhibits liver fibrosis.AIM To establish a network including transcriptomic and protein-protein interaction data to elucidate the molecular mechanism of taurine-induced HSC apoptosis.METHODS We used microarrays, bioinformatics, protein-protein interaction(PPI) network,and sub-modules to investigate taurine-induced changes in gene expression in human HSCs(LX-2). Subsequently, all of the differentially expressed genes(DEGs) were subjected to gene ontology function and Kyoto encyclopedia of genes and genomes pathway enrichment analysis. Furthermore, the interactions of DEGs were explored in a human PPI network, and sub-modules of the DEGs interaction network were analyzed using Cytoscape software.RESULTS A total of 635 DEGs were identified in taurine-treated HSCs when compared with the controls. Of these, 304 genes were statistically significantly up-regulated, and 331 down-regulated. Most of these DEGs were mainly located on the membrane and extracellular region, and are involved in the biological processes of signal transduction, cell proliferation, positive regulation of extracellular regulated protein kinases 1(ERK1) and ERK2 cascade, extrinsic apoptotic signaling pathway and so on. Fifteen significantly enriched pathways with DEGs were identified, including mitogen-activated protein kinase(MAPK) signaling pathway, peroxisome proliferators-activated receptor signaling pathway,estrogen signaling pathway, Th1 and Th2 cell differentiation, cyclic adenosine monophosphate signaling pathway and so on. By integrating the transcriptomics and human PPI data, nine critical genes, including MMP2, MMP9, MMP21,TIMP3, KLF10, CX3CR1, TGFB1, VEGFB, and EGF, were identified in the PPI network analysis.CONCLUSION Taurine promotes the apoptosis of HSCs via up-regulating TGFB1 and then activating the p38 MAPK-JNK-Caspase9/8/3 pathway. These findings enhance the understanding of the molecular mechanism of taurine-induced HSC apoptosis and provide references for liver disorder therapy.

Protective effects of taurine against muscle damage induced by diquat in 35 days weaned piglets

Background: Oxidative stress is a key factor that influences piglets' health. Taurine plays an imperative role in keeping the biological system from damage. This study was conducted to investigate the protective effect of taurine against muscle injury due to the secondary effect of diquat toxicity.Results: Our study found that taurine effectively and dose-dependently alleviated the diquat toxicity induced rise of feed/gain, with a concurrent improvement of carcass lean percentage. The plasma content of taurine was considerably increased in a dose-dependent manner. Consequently, dietary taurine efficiently improved the activity of plasma antioxidant enzymes. Furthermore, taurine attenuated muscle damage by restoring mitochondrial micromorphology, suppressing protein degradation and reducing the percentage of apoptotic cells in the skeletal muscle. Taurine supplementation also suppressed the genes expression levels of the antioxidant-, mitochondrial biogenesis-, and muscle atrophy-related genes in the skeletal muscle of piglets with oxidative stress.Conclusions: These results showed that the dose of 0.60% taurine supplementation in the diet could attenuate skeletal muscle injury induced by diquat toxicity. It is suggested that taurine could be a potential nutritional intervention strategy to improve growth performance.

Effect of taurine on immune function in mice with T-cell lymphoma during chemotherapy

ObjectiveTo observe the effect of taurine on immune function in mice with T-cell lymphoma during chemotherapy.MethodsA total of 40 C57BL/6 mice were selected and randomly divided into 4 groups, namely model group, chemotherapy group, taurine group and chemotherapy + taurine group, each containing 10 mice. Hypodermic injection was adopted to inoculate EL-4 cells in order to establish model of T-cell lymphoma. When the tumor achieved the size of 1 cm3, intervention treatments were given to the groups respectively. Mice in model group received 0.2 mL of normal saline which was intraperitoneally injected on Days 1, 8 and 15 with 3 weeks as a cycle; mice in chemotherapy group were administered with 80 mg/kg body weight of gemcitabine which was also intraperitoneally injected on Days 1, 8 and 15 with 3 weeks as a cycle; mice in taurine group were administered with 80 mg/kg body weight of taurine intraperitoneally injected daily for consecutive 8 d; mice in chemotherapy + taurine group were treated in the same manner as the mice in taurine group and chemotherapy group. Five mice were sacrificed at 2 and 3 weeks after intervention respectively, and the tumor tissues were collected and weighted after removal of auxiliary tissue, then the tumor inhibition rate was calculated. The thymus and spleen of mice sacrificed at 3 weeks after intervention were collected and weighted, and thymus and spleen indexes were calculated. Enzyme linked immunosorbent assay was used to detect the serum levels of IL-4, IL-10, IL-12 and IFN-γ in mice of each group.ResultsThe tumor weights in chemotherapy group, taurine group and chemotherapy + taurine group after 2 and 3 weeks of treatment were significantly lower than that in model group (P < 0.05); the tumor weight in chemotherapy + taurine group after 2 and 3 weeks of treatment was significantly lower than that in chemotherapy group (P < 0.05); the tumor inhibition rate in chemotherapy + taurine group was significantly higher than that in chemotherapy group and taurine group (P < 0.05); the thymus and spleen indexes in taurine group and chemotherapy + taurine group were significantly higher than those in chemotherapy group and model group (P < 0.05); the thymus and spleen indexes in chemotherapy group were significantly lower than those in model group (P < 0.05); after 3 weeks of treatment, the serum levels of IL-4, IL-12 and IFN-γ in chemotherapy group, taurine group and chemotherapy + taurine group were significantly lower than those in model group (P < 0.05); the IL-4 level in taurine group and chemotherapy + taurine group was significantly lower than that in chemotherapy group (P < 0.05); the serum level of IL-10 in chemotherapy group and chemotherapy + taurine group was significantly higher than that in model group and taurine group (P < 0.05); the serum level of IFN-γ in taurine group and chemotherapy + taurine group was significantly lower than that in model group and chemotherapy group (P < 0.05); after treatment of 3 weeks, the serum levels of IL-4 and IL-10 in chemotherapy group, taurine group and chemotherapy + taurine group were significantly lower than those in model group (P < 0.05), and IL-12 level was significantly higher than that in model group (P < 0.05); the level of IFN-γ in taurine group and chemotherapy + taurine group was significantly higher than that in model group (P < 0.05), while the level of IFN-γ in chemotherapy group was significantly lower than that in the other 3 groups (P < 0.05).ConclusionsTaurine can effectively enhance the immune function of mice with T-cell lymphoma during chemotherapy, reduce the toxicity of chemotherapy.

Metabolomic profiling for identification of metabolites and relevant pathways for taurine in hepatic stellate cells

AIM To develop a reliable and simple method to identify important biological metabolites and relevant pathways for taurine in hepatic stellate cells(HSCs), in order to provide more data for taurine therapy.METHODS All the biological samples were analyzed by using highperformance liquid chromatography-time electrospray ionization/quadrupole-time of flight mass spectrometry. Principal component analysis and partial least squares discriminant analysis were used to identify statistically different metabolites for taurine in HSCs, and metabolomic pathway analysis was used to do pathway analysis for taurine in HSCs. The chemical structure of the related metabolites and pathways was identified by comparing the m/z ratio and ion mode with the data obtained from free online databases.RESULTS A total of 32 significant differential endogenous metabolites were identified, which may be related to the mechanism of action of taurine in HSCs. Among the seven relevant pathways identified, sphingolipid metabolism pathway, glutathione metabolism pathway and thiamine metabolism pathway were found to be the most important metabolic pathways for taurine in HSCs.CONCLUSION This study showed that there were distinct changes in biological metabolites of taurine in HSCs and three differential metabolic pathways including sphingolipid pathway, glutathione pathway and thiamine metabolism pathway might be of key importance in mediating the mechanism of action of taurine in HSCs.

Taurine protects against retinal and optic nerve damage induced by endothelin-1 in rats via antioxidant effects

Endothelin-1（ET-1）, a potent vasoconstrictor, is involved in retinal vascular dysregulation and oxidative stress in glaucomatous eyes. Taurine（TAU）, a naturally occurring free amino acid, is known for its neuroprotective and antioxidant properties. Hence, we evaluated its neuroprotective properties against ET-1 induced retinal and optic nerve damage. ET-1 was administered intravitreally to Sprague-Dawley rats and TAU was injected as pre-, co-or post-treatment. Animals were euthanized seven days post TAU injection. Retinae and optic nerve were examined for morphology, and were also processed for caspase-3 immunostaining. Retinal redox status was estimated by measuring retinal superoxide dismutase, catalase, glutathione, and malondialdehyde levels using enzyme-linked immuosorbent assay. Histopathological examination showed significantly improved retinal and optic nerve morphology in TAU-treated groups. Morphometric examination showed that TAU pre-treatment provided marked protection against ET-1 induced damage to retina and optic nerve. In accordance with the morphological observations, immunostaining for caspase showed a significantly lesser number of apoptotic retinal cells in the TAU pre-treatment group. The retinal oxidative stress was reduced in all TAU-treated groups, and particularly in the pre-treatment group. The findings suggest that treatment with TAU, particularly pre-treatment, prevents apoptosis of retinal cells induced by ET-1 and hence prevents the changes in the morphology of retina and optic nerve. The protective effect of TAU against ET-1 induced retinal and optic nerve damage is associated with reduced retinal oxidative stress.