Taurine Administration Research Articles

Mitochondrial content is preserved throughout disease progression in the mdx mouse model of Duchenne muscular dystrophy, regardless of taurine supplementation.

Mitochondrial dysfunction is a pathological feature of Duchenne muscular dystrophy (DMD), a debilitating and fatal neuromuscular disorder characterized by progressive muscle wasting and weakness. Mitochondria are a source of cellular ATP involved in Ca2+ regulation and apoptotic signaling. Ameliorating aberrant mitochondrial function has therapeutic potential for reducing DMD disease severity. The dystrophic mdx mouse exhibits peak muscle damage at 21-28 days, which stabilizes after 8 wk. The amino acid taurine is implicated in mitochondrial health and function, with endogenous concentrations low when measured during the cycle of peak muscle damage in mdx mice. Using whole soleus and extensor digitorum longus (EDL) muscle homogenates from 28- and 70-day mdx mice, we found that there was no change in native state mitochondrial complexes using blue native-PAGE. NADH:ubiquinone oxidotreductase subunit-A9 (NDUFA9) protein abundance was lower in soleus muscle of 28- and 70-day mdx mice and EDL muscle of 70-day mdx mice compared with same muscles in WT (C57/BL10ScSn) animals. There were age-dependent increases in both NDUFA9 protein abundance and citrate synthase activity in soleus muscles of mdx and wild-type mice. There was no change in abundances of mitochondrial dynamics proteins mitofusin 2 (Mfn2) and mitochondrial dynamics protein 49 (MiD49). Taurine administration essentially did not affect any measurements of mitochondria. Collectively, these findings suggest mitochondrial content and dynamics are not reduced in the mdx mouse regardless of disease severity. We also elucidate that taurine affords no significant benefit to mitochondrial content or dynamics in the mdx mouse at either 28 or 70 days.

Taurine supplementation reduces neuroinflammation and protects against white matter injury after intracerebral hemorrhage in rats.

Intracerebral hemorrhage (ICH) initiates a neuroinflammatory cascade that contributes to substantial neuronal damage and neurological deterioration. Taurine, an abundant amino acid in the nervous system, is reported to reduce inflammatory injury in various central nervous system diseases, but its role and the possible underlying mechanisms in the pathology following ICH remains unclear. This study was designed to evaluate the effect of taurine supplementation on neurological deficits, acute inflammatory responses and white matter injury in a model of ICH in rats. Adult male Sprague-Dawley (SD) rats subjected to collagenase-induced ICH injury were injected intravenously with different concentrations of taurine or vehicle 10min after ICH and subsequently daily for 3days. Behavioral studies, brain water content, and assessments of hemorrhagic lesion volume were quantified at day 1 and day 3 post-ICH. Neuronal damage, peri-hematomal inflammatory responses, and white matter injury were determined at 24h, meanwhile, the content of hydrogen sulfide (H2S) along with the expression of cystathionine-β-synthase (CBS) and P2X7 receptor (P2X7R) in peri-hematomal tissues was analyzed to investigate the possible anti-inflammatory mechanism of taurine. Treatment with a high dosage of taurine (50mg/kg) significantly attenuated functional deficits and reduced brain edema and hemorrhagic lesion volume after ICH. Taurine administration also resulted in significant amelioration of neuronal damage and white matter injury. These changes were associated with marked reductions in neutrophil infiltration, glial activation, and expression levels of inflammatory mediators. Moreover, the anti-inflammatory effect of taurine was accompanied by increased H2S content, enhanced CBS expression, and less expression of P2X7R. Our study demonstrated that the high dosage of taurine supplementation effectively mitigated the severity of pathological inflammation and white matter injury after ICH, and the mechanism may be related to upregulation of H2S content and reduced P2X7R expression.

Taurine enhances spermatogenic function and antioxidant defense mechanisms in testes and epididymis of L-NAME-induced hypertensive rats

The beneficial health effects of taurine on hypertension have been demonstrated previously in both experimental and epidemiological studies. However, the role of taurine in reproductive dysfunction associated with hypertension has not been investigated. The present study evaluated the therapeutic efficacy of taurine on reproductive deficits in N-nitro-l-arginine methyl ester (L-NAME)-induced hypertensive rats. Sixty male Wistar rats were randomly assigned into six groups namely control, taurine alone, L-NAME alone (40mg/kg) or L-NAME treated with either taurine (100 and 200mg/kg) or reference drug atenolol (10mg/kg) for 28 consecutive days. Results indicated that taurine treatment significantly abrogated L-NAME-induced increase in systolic, diastolic and mean arterial pressures when compared with hypertensive control. Administration of taurine markedly increased antioxidant enzymes activities and glutathione level whereas it suppressed the increase in biomarkers of oxidative stress in the testes and epididymis of L-NAME-induced hypertensive rats. Moreover, taurine significantly reversed hypertension mediated decreases in circulatory concentrations of luteinizing hormone, follicle-stimulating hormone and testosterone whereas it increased testicular sperm number, epididymal sperm number and sperm progressive motility in the hypertensive rats. Furthermore, taurine abrogated the suppression of marker enzymes of testicular function namely acid phosphatase, alkaline phosphatase and lactate dehydrogenase and preserved the histo-architectures of the testes and epididymis in L-NAME-induced hypertensive rats. Taken together, the findings from this study highlight the beneficial role of taurine in reproductive system of L-NAME-induced male hypertensive rats. Taurine supplementation may be a good clinical approach to prevent reproductive deficits in male hypertensive patients.

Energy Drink Doses of Caffeine and Taurine Have a Null or Negative Effect on Sprint Performance.

Jeffries, O, Hill, J, Patterson, SD, and Waldron, M. Energy drink doses of caffeine and taurine have a null or negative effect on sprint performance. J Strength Cond Res 34(12): 3475-3481, 2020-This study investigated the effects of caffeine and taurine coingestion on repeat-sprint cycling performance and associated physiological and perceptual responses. In a double-blind, cross-over, repeated measures study, 11 male subjects (age 21 ± 2 years; stature 178 ± 7 cm; body mass 80 ± 13 kg) completed 10 × 6-second sprints on a cycle ergometer, each separated by 24 seconds, one hour after ingesting: caffeine (80 mg) and taurine (1 g), equivalent to the amount observed in popular commercial energy drinks, or placebo (maltodextrin ∼1 g) in a gelatine capsule. Performance was measured on a cycle ergometer, whereas blood lactate concentration (B[la]), rating of perceived exertion (RPE), and heart rate (HR) were measured at baseline (pre-exercise) and after sprints 5 and 10. Magnitude-based inferences revealed likely, trivial differences in peak power and unclear, trivial intersprint fatigue index after ingestion of the caffeine and taurine supplement. Intrasprint fatigue was greater in the caffeine and taurine condition at sprint 10 (likely, small) and possibly smaller in sprints 6-9. The caffeine and taurine supplement had a likely large effect on HR at baseline (effect size = 0.94) and increases in B[la] after sprints 5 (likely small) and 10 (possibly small). There was no effect of the supplement on RPE (unclear, trivial). Administration of caffeine and taurine at doses equivalent to commercial energy drinks did not improve repeat-sprint cycling performance and seemed to induce greater fatigue within selected sprints, particularly at the end of the trial. This undesirable performance effect occurs in parallel with increased HR and glycolytic metabolic bi-products.

Protective effects of taurine on growth performance and intestinal epithelial barrier function in weaned piglets challenged without or with lipopolysaccharide

We evaluated whether weaned piglets were protected from bacterial endotoxins by placing the animals on a taurine-supplemented diet. A total of 40 weaned Landrace × Yorkshire piglets (5.75 ± 0.58 kg, weaned at 21 days) were allocated to four groups with 10 barrows per group, following a 2 × 2 factorial design with two inclusion levels of lipopolysaccharide (LPS) (no or one time peritoneal injection by the dose of 100 µg/kg bodyweight on Day 7 of the trial) and two inclusion levels of dietary taurine (no or 0.1% taurine in a basal diet in the whole trial). There was a significant interaction between LPS and taurine with regard to growth and small intestinal mucosal membrane integrity, morphology, immune parameters, and antioxidant capacity (P < 0.05). Feed conversion, daily weight gain, daily feed intake, villus height, and the villus to crypt ratio, vascular endothelial growth factor, regenerating islet-derived protein 3 gamma, trefoil factor-3, transforming growth factor β-1 expression, number of goblet cells and the least amount of claudin-1, occludin, zonula occludens-1, serum glutathione peroxidase, nitrogen oxide synthase, superoxide dismutase, peroxidase, and total antioxidant was lowest in LPS-challenged animals. Furthermore, animals in the LPS group had the highest serum diamine oxidase concentration, number of lymphocytes, concentrations of calprotectin, sIgA, toll-like receptor-4, mRNA levels of interleukin-1β, interleukin-8, toll-like receptor-4, and tumour necrosis factor-α (P < 0.05). These data suggested that the peritoneal injection administration of LPS decreased growth performance and disrupted small intestinal mucosal membrane integrity and triggered an inflammatory response in the small intestinal mucosal membrane. Dietary administration of taurine improved growth performance, increased small intestinal villus height, stimulated immune and antioxidant function and improved small intestinal mucosal membrane integrity in weaned piglets challenged without or with LPS (P < 0.05). The beneficial effects of taurine were likely due to decreased stimulation of the immune response to LPS and an improvement in intestinal epithelial barrier function. Dietary administration of taurine could prevent weaned piglets from intestinal damage by LPS of Gram-negative bacteria.

Role of myeloperoxidase in abdominal aortic aneurysm formation: mitigation by taurine.

Oxidative stress plays a fundamental role in abdominal aortic aneurysm (AAA) formation. Activated polymorphonuclear leukocytes (or neutrophils) are associated with AAA and express myeloperoxidase (MPO), which promotes inflammation, matrix degradation, and other pathological features of AAA, including enhanced oxidative stress through generation of reactive oxygen species. Both plasma and aortic MPO levels are elevated in patients with AAA, but the role of MPO in AAA pathogenesis has, heretofore, never been investigated. Here, we show that MPO gene deletion attenuates AAA formation in two animal models: ANG II infusion in apolipoprotein E-deficient mice and elastase perfusion in C57BL/6 mice. Oral administration of taurine [1% or 4% (wt/vol) in drinking water], an amino acid known to react rapidly with MPO-generated oxidants like hypochlorous acid, also prevented AAA formation in the ANG II and elastase models as well as the CaCl2 application model of AAA formation while reducing aortic peroxidase activity and aortic protein-bound dityrosine levels, an oxidative cross link formed by MPO. Both MPO gene deletion and taurine supplementation blunted aortic macrophage accumulation, elastin fragmentation, and matrix metalloproteinase activation, key features of AAA pathogenesis. Moreover, MPO gene deletion and taurine administration significantly attenuated the induction of serum amyloid A, which promotes ANG II-induced AAAs. These data implicate MPO in AAA pathogenesis and suggest that studies exploring whether taurine can serve as a potential therapeutic for the prevention or treatment of AAA in patients merit consideration.NEW & NOTEWORTHY Neutrophils are abundant in abdominal aortic aneurysm (AAA), and myeloperoxidase (MPO), prominently expressed in neutrophils, is associated with AAA in humans. This study demonstrates that MPO gene deletion or supplementation with the natural product taurine, which can scavenge MPO-generated oxidants, can prevent AAA formation, suggesting an attractive potential therapeutic strategy for AAA.

Protective effects of taurine against renal ischemia/reperfusion injury in rats by inhibition of gelatinases, MMP-2 and MMP-9, and p38 mitogen-activated protein kinase signaling

Dysregulated expression of matrix metalloproteinases (MMPs) is closely associated with the pathogenesis of renal ischemia/reperfusion injury (I/R). The production of excessive reactive oxygen species (ROS) causes tissue damage. Increased ROS production causes activation of p38 mitogen-activated protein kinase (MAPK) signaling, which participates in gene regulation of MMPs, especially MMP-2 and MMP-9 (gelatinases). Taurine (2-aminoethanesulfonic acid) in mammalian cells functions in bile acid conjugation, maintenance of calcium homeostasis, osmoregulation, membrane stabilization, and antioxidation, antiinflammatory, and antiapoptotic action. We investigated the effects of taurine and the possible role of p38 MAPK signaling on regulation of MMP-2 and MMP-9 in a renal I/R injury model in rats. Rats were divided into three groups: sham, I/R, and I/R + taurine treated. After a right nephrectomy, I/R was induced by clamping the left renal pedicle for 1 h followed by 6 h reperfusion. Taurine was administered 45 min prior to induction of ischemia. Renal function was assessed by serum creatinine and blood urea nitrogen (BUN) levels. Tubule injury and structural changes were evaluated by light microscopy. Malondialdehyde (MDA) levels were analyzed by high performance liquid chromatography (HPLC). Superoxide dismutase (SOD) activity levels were measured using a colorimetric kit. mRNA expression of MMP-2 and MMP-9 was determined by real-time polymerase chain reaction. MMP-2 and MMP-9 activities were measured using a fluorimetric kit. Phosphorylated p38 (p-p38) and total p38 MAPK protein expressions were evaluated by western blot. Taurine pretreatment significantly attenuated renal dysfunction and histologic damage, such as renal tubule dilation and loss of brush borders. The pretreatment also decreased the MDA level and attenuated the reduction of SOD activity in the kidney during I/R. Taurine pretreatment also decreased significantly both MMP-2 and MMP-9 mRNA expression and MMP-9 activity induced by I/R. In addition, the activity of p38 MAPK signaling was down-regulated significantly by taurine administration. Inhibition of MMP-2 and MMP-9 expression and MMP-9 activity caused by taurine may be associated with suppression of p38 MAPK activation during I/R induced renal injury in rats. Therefore, taurine administration may prove to be a strategy for attenuating renal I/R injury.

Taurine restores the exploratory behavior following alcohol withdrawal and decreases BDNF mRNA expression in the frontal cortex of chronic alcohol-treated rats

Alcohol use disorder is an alarming health problem, and the withdrawal symptoms increase the risk of relapse. We have hypothesized that taurine, a multitarget substance acting as a gamma-aminobutyric acid A receptor (GABAAR) positive modulator and a partial inhibitor of N-methyl-d-aspartate (NMDA) glutamate receptors, may reduce the withdrawal symptoms or modify behaviors when combined with alcohol. Therefore, we investigated the effects of taurine on behavior in the open field test (OFT), the GABAAR α2 subunit and BDNF mRNA expression in the frontal cortex of rats after chronic alcohol treatment or upon withdrawal. Rats received alcohol 2g/kg (alcohol and withdrawal groups) or water (control group) twice daily by oral gavage for 28days. On day 29, the withdrawal rats received water instead of alcohol, and all groups were reallocated to receive 100mg/kg taurine or vehicle intraperitoneally, once a day for 5days. On day 33, the rats were exposed to OFT; 18h later, they were euthanized, and the frontal cortex was dissected for GABAAR α2 subunit detection and BDNF mRNA expression determination by real-time quantitative PCR. Taurine administration restored rearing behavior to the control levels in the withdrawal rats. Taurine also showed anxiolytic-like effects in control rats and did not change the behaviors in the chronic alcohol group. Chronic alcohol treatment or withdrawal did not change the GABAAR α2 subunit or BDNF mRNA expression in the frontal cortex, but taurine decreased the α2 subunit level in control rats and to the BDNF levels in the alcohol rat group. We conclude that taurine restored exploratory behavior after alcohol withdrawal but that this effect was not related to the GABAAR α2 subunit or BDNF mRNA expression in the frontal cortex of the rats.

Effects of taurine on resting-state fMRI activity in spontaneously hypertensive rats.

Attention deficit hyperactivity disorder (ADHD) is a global behavior illness among children and adults. To investigate the effects of taurine on resting-state fMRI activity in ADHD, a spontaneously hypertensive rat (SHR) animal model was adopted. Significantly decreased serum C-reactive protein (CRP) was detected in rats of Wistar Kyoto (WKY) high-taurine group and significantly decreased interleukin (IL)-1β and CRP were detected in rats of SHR low-taurine and high-taurine groups. Moreover, significantly higher horizontal locomotion was detected in rats of WKY low-taurine and SHR low-taurine groups than in those of controls. In contrast, significantly lower horizontal locomotion was detected in rats of the SHR high-taurine group than in those of the SHR control group. Additionally, significantly lower functional connectivity (FC) and mean amplitude of low-frequency fluctuation (mALFF) in the bilateral hippocampus in rats of WKY high-taurine and SHR high-taurine groups was detected. Notably, the mALFF in rats of the SHR low-taurine and high-taurine groups was significantly lower than in those of the SHR control group. These findings suggest that the administration of a high-dose taurine probably improves hyperactive behavior in SHR rats by ameliorating the inflammatory cytokines and modulating brain functional signals in SHR rats.

Protective role of taurine against hepatotoxicity induced by pyrazinamide in rats

Background: Pyrazinamide is a widely used antituberculosis drug. However, associated with its clinical use, hepatotoxicity is a life-threating side effect reported in some patients, but the exact mechanism by which pyrazinamide induces hepatotoxicity is not clear yet. Aims and Objectives: The present investigation was conducted to study the exact mechanism of subchronic toxicity induced by pyrazinamide and protective role of taurine in rats. Materials and Methods: Markers such as alanine transaminase (ALT) and aspartate aminotransferase (AST) levels, lipid peroxidation, reactive oxygen species (ROS) formation, hepatocytes glutathione (GSH) content, and apoptosis were examined. Furthermore, pathological changes were evaluated. Results: The results showed that pyrazinamide administration caused hepatotoxicity as revealed by elevation in ALT and AST levels. Pyrazinamide increased ROS generation and malondialdehyde derivative levels, and also, it reduced intracellular GSH contents. Pyrazinamide induced apoptosis in rats liver tissue. Conclusion: Administration of taurine effectively decreased the intensity of hepatotoxicity induced by pyrazinamide in rats.

The potential protective role of taurine against experimental allergic inflammation

AimsTaurine has been widely evaluated as a potential therapeutic agent in chronic inflammatory disorders and various infections. However, the potential role of taurine in regulating allergic inflammatory responses is currently unknown. Materials and methodsThe present study was designed to evaluate the in vitro effects of taurine on the levels of thymic stromal lymphopoietin (TSLP) and other pro-inflammatory cytokines and activation of caspase-1 and nuclear factor (NF)-κB as well as the phosphorylations of c-Jun N-terminal kinase (JNK) and p38 in phorbol 12-myristate 13-acetate and calcium ionophore A23187 (PMACI)-triggered human mast cell line, HMC-1 cells. Furthermore, we assessed the therapeutic effects of taurine on ovalbumin (OVA)-induced allergic rhinitis (AR) animal models. Key findings and significanceHere, the obtained results showed that taurine dose-dependently inhibited the production and mRNA expression of TSLP and pro-inflammatory cytokines in HMC-1 cells exposed to PMACI. Taurine attenuated the phosphorylation of JNK and p38 in activated HMC-1 cells. Moreover, taurine brought a significant inhibition of the activities of NF-κB and caspase-1. In an OVA-induced AR animal model, the increased levels of nose rubbing, histamine, immunoglobulin E, TSLP, and interleukin IL-1β were dramatically reduced by the administration of taurine. In summary, taurine could serve as potential novel remedy of allergic inflammatory disorders.

Pengaruh Pemberian Taurin terhadap Gambaran Histopatologi Paru Mencit (Mus musculus) yang Diinduksi Karsinogen Benzo(α)Piren secara In Vivo

Lung cancer is a disease that causes high mortality. Drugs used to prevent and cure cancer mostly causes intoxicity to the normal tissues due to its less effectiveness. Therefore, it is necessary to find out any agent or substance which works much more effective and safe for cancer treatment. The aim of the study was to elucidate the role of taurine on the lung tissue of mice (Mus musculus) induced by carcinogenic benzo(α)pyrene. The experiment was conducted in a completely randomized design with 5 replications. Six treatment groups were perfomed. Group I was given 0.2 mL of corn oil and given aquadest until the end of the study period, group II was induced by benzo(α)pyrene without administration of taurine, group III before induced with benzo(α)pyrene, was given taurine dosage 7.8 mg/BW/day for two weeks, group IV after induced benzo(α)pyrene, was given taurine with dosage 3.9 mg/BW/day, group V after induced benzo(α)pyrene, was given taurine with dosage7. 8 mg/BW/day, group VI after induced with benzo(α)pyrene, was given taurine with dosage 15.6 mg/BW/day. The results of the Kruskal-Wallis analysis and one way ANOVA with LSD (p>0,05) showed that taurine reduced lung tissue damage 72.73% due to the administration of benzo(α)pyrene of 0.3 mg/BW/day. In addition, the effective dose of taurine reduce lung tissue damage was 15.6 mg/BW/day.

Supplementation with Phycocyanobilin, Citrulline, Taurine, and Supranutritional Doses of Folic Acid and Biotin-Potential for Preventing or Slowing the Progression of Diabetic Complications.

Oxidative stress, the resulting uncoupling of endothelial nitric oxide synthase (eNOS), and loss of nitric oxide (NO) bioactivity, are key mediators of the vascular and microvascular complications of diabetes. Much of this oxidative stress arises from up-regulated nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity. Phycocyanobilin (PhyCB), the light-harvesting chromophore in edible cyanobacteria such as spirulina, is a biliverdin derivative that shares the ability of free bilirubin to inhibit certain isoforms of NADPH oxidase. Epidemiological studies reveal that diabetics with relatively elevated serum bilirubin are less likely to develop coronary disease or microvascular complications; this may reflect the ability of bilirubin to ward off these complications via inhibition of NADPH oxidase. Oral PhyCB may likewise have potential in this regard, and has been shown to protect diabetic mice from glomerulosclerosis. With respect to oxidant-mediated uncoupling of eNOS, high-dose folate can help to reverse this by modulating the oxidation status of the eNOS cofactor tetrahydrobiopterin (BH4). Oxidation of BH4 yields dihydrobiopterin (BH2), which competes with BH4 for binding to eNOS and promotes its uncoupling. The reduced intracellular metabolites of folate have versatile oxidant-scavenging activity that can prevent oxidation of BH4; concurrently, these metabolites promote induction of dihydrofolate reductase, which functions to reconvert BH2 to BH4, and hence alleviate the uncoupling of eNOS. The arginine metabolite asymmetric dimethylarginine (ADMA), typically elevated in diabetics, also uncouples eNOS by competitively inhibiting binding of arginine to eNOS; this effect is exacerbated by the increased expression of arginase that accompanies diabetes. These effects can be countered via supplementation with citrulline, which efficiently enhances tissue levels of arginine. With respect to the loss of NO bioactivity that contributes to diabetic complications, high dose biotin has the potential to “pinch hit” for diminished NO by direct activation of soluble guanylate cyclase (sGC). High-dose biotin also may aid glycemic control via modulatory effects on enzyme induction in hepatocytes and pancreatic beta cells. Taurine, which suppresses diabetic complications in rodents, has the potential to reverse the inactivating impact of oxidative stress on sGC by boosting synthesis of hydrogen sulfide. Hence, it is proposed that concurrent administration of PhyCB, citrulline, taurine, and supranutritional doses of folate and biotin may have considerable potential for prevention and control of diabetic complications. Such a regimen could also be complemented with antioxidants such as lipoic acid, N-acetylcysteine, and melatonin—that boost cellular expression of antioxidant enzymes and glutathione—as well as astaxanthin, zinc, and glycine. The development of appropriate functional foods might make it feasible for patients to use complex nutraceutical regimens of the sort suggested here.

Chronic treatment with taurine after intracerebroventricular streptozotocin injection improves cognitive dysfunction in rats by modulating oxidative stress, cholinergic functions and neuroinflammation

The present study investigated the neuroprotective effects of taurine, an essential amino acid for growth and development of central nervous system. Intracerebroventricular streptozotocin (ICV-STZ) model of cognitive impairment was used in male Wistar rats (270 ± 20 g). Morris water maze, elevated plus maze and passive avoidance paradigm were used to assess cognitive performance. Taurine (40, 60 and 120 mg/kg) was administered orally for 28 days following STZ administration on day 1. Oxidative stress parameters (malondialdehyde, glutathione, nitric oxide and superoxide dismutase) and cholinesterases (acetylcholinesterase and butyrylcholinesterase) activity were measured at end of the study in the cortex and hippocampus. Levels of TNF-α, IL-1β, expression of rho kinase-II (ROCK-II), glycogen synthase kinase-3β (GSK-3β) and choline acetyltransferase (ChAT) were studied in cortex and hippocampus. STZ caused significant cognitive impairment as compared to normal control. Chronic administration of taurine attenuated STZ-induced cognitive impairment. Increased oxidative stress and increased levels of TNF-α, IL-1β induced by STZ were also significantly attenuated by taurine. Taurine significantly (p < 0.05) decreased the STZ-induced increased expression of ROCK-II in cortex and hippocampus. Further, STZ-induced increased activity of cholinesterases was significantly (p < 0.001) mitigated by taurine. STZ decreased the expression of ChAT in hippocampus which was significantly (p < 0.05) reversed by taurine. However, GSK-3β expression was not altered by either STZ or taurine. The present study indicates that taurine exerts a neuroprotective role against STZ-induced cognitive impairment in rats. This effect is probably mediated by modulating oxidative stress, cholinesterases, inflammatory cytokines and expression of ROCK-II. Thus, this study suggests a potential of chronic taurine administration in cognitive impairment of Alzheimer's type.

Taurine Reverses Atrial Structural Remodeling in Ach-Cacl2 Induced Atrial Fibrillation Rats.

Taurine has been reported to have anti-arrhythmia effects, but the anti-atrial fibrillation (AF) effects and its mechanism remain incompletely understood. In the present study, the therapy effects and partly mechanisms were investigated. AF animal model was established by intravenous administered with the mixture of acetylcholine (Ach) and CaCl2 (66 μg/mL + 10 mg/mL) (i.v.) for 7 days. The actions of taurine (99 mg/kg∙d, introgastric administration) on the levels of Hs-CRP, IL-6, TNF-α, MMP-9, AngII, the extent of the fibrosis and ultrastructural changes in left atrial were studied. The data showed that the serum levels of TNF-α, IL-6, AngII and the plasma levels of Hs-CRP and MMP-9 were significantly elevated in automatic recovery group relative to the control group (p < 0.01), which were all decreased by taurine administration (p < 0.01) similar to Verapamil treatment. Masson's trichrome staining of the left atrial tissue showed an obvious interstitial fibrosis in rats of automatic recovery group. The alteration could be reversed by additional taurine. Electron microscopy revealed that taurine administration could significantly alleviate the ultrastructural damage of atrial cells, and the effects were similar to the Verapamil treatment. In conclusion, the results suggested that taurine could inhibit the structural remodeling of AF in rats partly by decreasing the levels of inflammatory factors and profibrotic molecules, attenuating the extent of myocardial fibrosis and protecting the integrity of myocardial ultrastructure.

Taurine Directly Binds to Oligomeric Amyloid-β and Recovers Cognitive Deficits in Alzheimer Model Mice.

Alzheimer's disease (AD) is the most common cause of dementia leading to severe cognitive decline. During the progression of AD, amyloid-β (Aβ) monomers aggregate into neurotoxic soluble oligomeric Aβ that causes cognitive impairments. Our previous study indicates that oral supplementation of taurine at 1000mg/kg/day significantly ameliorates hippocampal-dependent cognitive deficits in APP/PS1 transgenic AD mouse model. However, Aβ plaques and oligomeric Aβ levels are not affected after administration of taurine and the oral dosage of taurine was relatively high. Thus, in this study, we focused on direct correlation between taurine and oligomeric Aβ, causing memory deficits in a lower oral dosage of taurine, 250mg/kg/day. We induced AD-like cognitive impairments to adult normal mice and orally administered taurine via drinking water for 10days. We confirmed that taurine administration improved cognitive deficits in oligomeric Aβ-infusion mice in Y-maze and passive avoidance tests without activity alteration of mice. In addition, we found that taurine directly bound to oligomeric Aβ in surface plasmon resonance analyses. Our results propose that taurine can ameliorate cognitive impairment by directly binding to oligomeric Aβ in oral administration of 250mg/kg/day for 10days.

Taurine Improves Sexual Function in Streptozotocin-Induced Diabetic Rats.

Previous studies have identified that diabetic erectile dysfunction is associated with androgen and nitric oxide deficiency resulting from hyperglycemia. It has been demonstrated that taurine can stimulate testosterone secretion, increase nitric oxide synthase (NOS) activity and nitric oxide (NO) production, and reduce blood glucose levels in the diabetic animals. Furthermore, recent studies have found that taurine relaxes both the corpus cavernosum and the vasculature. Accordingly, we hypothesized that taurine might exert beneficial effects on erectile function of the diabetic rats. Here, we assessed the effects of taurine on sexual function in streptozotocin (STZ) -induced diabetic male rats. We observed that taurine treatment could markedly increase sexual response and mating ability of STZ-diabetic rats. The serum concentration of gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH), follicle-stimulating hormone (FSH) and testosterone (T) were also significantly increased by taurine administration. Importantly, taurine supplementation notably increased mRNA levels and activity of endothelial NOS (eNOS) and neuronal NOS (nNOS), as well as NO and cGMP content, in the corpus cavernosum of the diabetic rats. In conclusion, the present data indicate that taurine can increase sexual function of STZ-induced diabetic male rats mainly by correcting the diabetes, increasing sexual desire, which is implicated in ameliorating the hypothalamic-pituitary-testicular axis function, and by improving penile erection, which requires increased signaling from the penile endothelial- and neuronal-dependent NO-cGMP pathway.

Taurine Increases Insulin Expression in STZ-Treated Rat Islet Cells In Vitro.

This research aims at figure out the effects and the pathway of taurine on insulin in islet cells cultured in vitro treated by STZ. In the experiment, islet cells were isolated from pancreatic tissue by in situ perfusion with collagenase V. The pancreatic islet cells, maintained in RPMI 1640 culture medium were divided into six groups: C: control, E: supplemented with 10mmol/L of taurine, group M, T1, T2 and T3 was treated with STZ (0.5mmol/L), at the same time, taurine were added in group T1,T2 and T3 for 30min, and then culture medium were collected by centrifugation and then insulin levels were detected by radioimmunoassay, the cells were then rinsed with Hanks, and 0,10, 0, 5, 10, 20mmol/L of taurine in group C, E, M, T1, T2 and T3 were added for 24h respectively. Total RNA was extracted, then insulin gene and its transcription regulator such as PDX-1, NeuroD1 were amplified by semi-quantitative RT-PCR. The results showed that, the release of insulin from islet cells treated by STZ could be inhibited by taurine, gene expression of insulin, PDX-1 and NeuroD1 in STZ group decreased significantly, which were up-regulated by taurine administration. In conclusion, taurine exerts a certain degree of protective and reconstructive effects on islet cells treated by STZ.

Ammonia-induced mitochondrial dysfunction and energy metabolism disturbances in isolated brain and liver mitochondria, and the effect of taurine administration: relevance to hepatic encephalopathy treatment

IntroductionAmmonia-induced oxidative stress, mitochondrial dysfunction, and energy crisis are known as some the major mechanisms of brain injury in hepatic encephalopathy (HE). Hyperammonemia also affects the liver and hepatocytes. Therefore, targeting mitochondria seems to be a therapeutic point of intervention in the treatment of HE. Taurine is an abundant amino acid in the human body. Several biological functions including the mitochondrial protective properties are attributed to this amino acid. The aim of this study is to evaluate the effect of taurine administration on ammonia-induced mitochondrial dysfunction.Material and methodsIsolated mice liver and brain mitochondria were exposed to different concentrations of ammonia (1, 5, 10, and 20 mM) and taurine (1, 5, and 10 mM), and several mitochondrial indices were assessed.ResultsIt was found that ammonia inhibited mitochondrial dehydrogenases activity caused collapse of mitochondrial membrane potential (MMP), induced mitochondrial swelling (MPP), and increased reactive oxygen species (ROS) in isolated liver and brain mitochondria. Furthermore, a significant amount of lipid peroxidation (LPO), along with glutathione (GSH) and ATP depletion, was detected in ammonia exposed mitochondria. Taurine administration (5 and 10 mM) mitigated ammonia-induced mitochondrial dysfunction.ConclusionsThe current investigation demonstrates that taurine is instrumental in preserving brain and liver mitochondrial function in a hyperammonemic environment. The data suggest taurine as a potential protective agent with a therapeutic capability against hepatic encephalopathy and hyperammonemia.

Taurine Recovers Testicular Steroidogenesis and Spermatogenesis in Streptozotocin-Induced Diabetic Rats.

A great deal of investigations have verified that diabetic male reproductive impairment is associated with the dysfunction of testicular steroidogenesis and spermatogenesis resulted from insulin deficiency and hyperglycaemia-induced oxidative stress. It has been identified taurine is profitable for diabetes mellitus and diabetic implications through its insulin-like and islet cells protective activity. Furthermore, our previous studies found that taurine could increase testicular antioxidative ability, stimulate the endocrine activity of hypothalamic-pituitary-testicular axis, elevate testosterone level, raise sperm quality, suppress the deterioration of testicular function. Accordingly, we hypothesized that taurine may have beneficial effects on testicular dysfunction under diabetic mellitus status. Here, we investigated the effects of taurine on testicular steroidogenesis and spermatogenesis in streptozotocin (STZ)-induced type I diabetic rats. We observed that taurine treatment can markedly increase the body and testis weights, testicular SDH and G6PDH activities, decrease the serum fasting glucose concentration of diabetic rats. Serum contents of GnRH, LH, FSH, T, and testicular StAR, 3β-HSD, 17β-HSD mRNA expression levels were also obviously raised by taurine administration, indicating that taurine can improve testicular steroidogenesis in diabetic animals. Finally, we found taurine supplementation effectively elevated the sperm count and motility, reduced sperm abnormality, suggesting that taurine can increase the testicular spermatogenesis function of diabetic rat. In summary, the present data indicated that taurine can rescue the function of testicular steroidogenesis and spermatogenesis in STZ-induced type I diabetic rats possibly by increasing the endocrine activity of hypothalamic-pituitary-testicular axis.