Protective Role Of Taurine Research Articles

Protective Role of Taurine on Rat Offspring Hypertension in the Setting of Maternal Chronic Kidney Disease.

Taurine is a natural antioxidant with antihypertensive properties. Maternal chronic kidney disease (CKD) has an impact on renal programming and increases the risk of offspring hypertension in later life. The underlying mechanisms cover oxidative stress, a dysregulated hydrogen sulfide (H2S) system, dysbiotic gut microbiota, and inappropriate activation of the renin-angiotensin-aldosterone system (RAAS). We investigated whether perinatal taurine administration enables us to prevent high blood pressure (BP) in offspring complicated by maternal CKD. Before mating, CKD was induced through feeding chow containing 0.5% adenine for 3 weeks. Taurine was administered (3% in drinking water) during gestation and lactation. Four groups of male offspring were used (n = 8/group): controls, CKD, taurine-treated control rats, and taurine-treated rats with CKD. Taurine treatment significantly reduced BP in male offspring born to mothers with CKD. The beneficial effects of perinatal taurine treatment were attributed to an augmented H2S pathway, rebalance of aberrant RAAS activation, and gut microbiota alterations. In summary, our results not only deepen our knowledge of the mechanisms underlying maternal CKD-induced offspring hypertension but also afford us the impetus to consider taurine-based intervention as a promising preventive approach for future clinical translation.

The hepatoprotective effects of taurine against oxidative stress induced by isotretinoin in rats.

Liver disorders are one of the principal reasons for mortality in the world. Isotretinoin is a systemic retinoid that has been approved for therapy of acne vulgaris since 1982. This drug causes complications in the body. Evidence suggests that Isotretinoin might cause hepatotoxicity. Our research aimed to study the exact mechanism of hepatotoxicity induced by isotretinoin and the protective role of taurine in this toxicity. Biomarkers such as aspartate transaminase (AST) and alanine transaminase (ALT), superoxide dismutase, glutathione content (GSH), catalase,and malondialdehyde (MDA) were examined. Furthermore, pathological changes were evaluated. The results showed that oral administration of Isotretinoin induced hepatotoxicity as showed by elevation in ALT, AST, and MDA; also, it reduced intracellular GSH in rat liver tissue. Administration of taurine prevented the hepatotoxicity induced by isotretinoin in rats significantly.

Endoplasmic reticulum stress and mitochondrial injury are critical molecular drivers of AlCl3-induced testicular and epididymal distortion and dysfunction: protective role of taurine

Aluminum, the third most plentiful metal in the Earth’s crust, has potential for human exposure and harm. Oxidative stress plays an essential role in producing male infertility by inducing defects in sperm functions. We aimed to investigate the role of endoplasmic reticulum (ER) stress and mitochondrial injury in the pathogenesis of aluminum chloride (AlCl3)-induced testicular and epididymal damage at the histological, biochemical, and molecular levels, and to assess the potential protective role of taurine. Forty-eight adult male albino rats were separated into four groups (12 in each): negative control, positive control, AlCl3, and AlCl3 plus taurine groups. Testes and epididymis were dissected. Histological and immunohistochemical (Bax and vimentin) studies were carried out. Gene expression of vimentin, PCNA, CHOP, Bcl-2, Bax, and XBP1 were investigated via quantitative real-time polymerase chain reaction (qRT-PCR), besides estimation of malondialdehyde (MDA) and total antioxidant capacity (TAC). Light and electron microscopic examinations of the testes and epididymis revealed pathological changes emphasizing both mitochondrial injury and ER stress in the AlCl3 group. Taurine-treated rats showed a noticeable improvement in the testicular and epididymal ultrastructure. Moreover, they exhibited increased gene expression of vimentin, Bcl-2, and PNCA accompanied by decreased CHOP, Bax, and XBP1 gene expression. In conclusion, male reproductive impairment is a significant hazard associated with AlCl3 exposure. Both ER stress and mitochondrial impairment are critical mechanisms of the deterioration in the testes and epididymis induced by AlCl3, but taurine can amend this.

Cadmium induces placental glucocorticoid barrier damage by suppressing the cAMP/PKA/Sp1 pathway and the protective role of taurine

Cadmium (Cd) exposure during pregnancy damages the placental glucocorticoid (GC) barrier, exposes the foetus to excess corticosterone (CORT) levels, and eventually inhibits foetal development. In addition, taurine (Tau) alleviates the toxicity of Cd on liver and kidney, but limited data are available on the role of Tau against the toxicity of heavy metals on female reproduction and fetal development. The present study was conducted to investigate the specific mechanism of Cd-induced placental GC barrier damage and the protective role of Tau. Pregnant rats were administered CdCl2 (1 mg/kg/day) and Tau (100, 200, or 300 mg/kg/day) by gavage from gestational day (GD) 0 to 19. The data showed that CdCl2 increased the foetal growth restriction (FGR) rate of the offspring, and the levels of CORT in the placental, maternal and foetal serum. Treatment with Tau significantly reversed the impact of Cd on both maternal and fetal parameters. Additionally, Tau can attenuate Cd-induced inhibition of 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2) and specificity protein 1 (Sp1) in vivo and vitro. Furthermore, Sp1-siRNA alone reduced 11β-HSD2 levels and had a further inhibitory effect when the cells were treated with Cd simultaneously. Moreover, Cd suppressed cAMP/PKA signalling. Forskolin (adenylate cyclase agonist) pretreatment activated cAMP/PKA signalling and restored the Cd-induced downregulation of Sp1 and 11β-HSD2. Tau alleviated the Cd-induced decrease of Sp1 via activating cAMP/PKA signalling. Therefore, the results highlight that Tau protects against Cd-induced impairments in GC barrier damage by upregulating the cAMP/PKA/Sp1 pathway in placental trophoblasts.

Protective role of taurine against oxidative stress (Review).

Taurine is a fundamental mediator of homeostasis that exerts multiple roles to confer protection against oxidant stress. The development of hypertension, muscle/neuro- associated disorders, hepatic cirrhosis, cardiac dysfunction and ischemia/reperfusion are examples of some injuries that are linked with oxidative stress. The present review gives a comprehensive description of all the underlying mechanisms of taurine, with the aim to explain its anti-oxidant actions. Taurine is regarded as a cytoprotective molecule due to its ability to sustain normal electron transport chain, maintain glutathione stores, upregulate anti-oxidant responses, increase membrane stability, eliminate inflammation and prevent calcium accumulation. In parallel, the synergistic effect of taurine with other potential therapeutic modalities in multiple disorders are highlighted. Apart from the results derived from research findings, the current review bridges the gap between bench and bedside, providing mechanistic insights into the biological activity of taurine that supports its potential therapeutic efficacy in clinic. In the future, further clinical studies are required to support the ameliorative effect of taurine against oxidative stress.

Developmental toxicity of lead in rats after gestational exposure and the protective role of taurine.

The present study was conducted to investigate the potential adverse effect of Pb on pregnant Sprague-Dawley rats and their fetuses after maternal exposure, on gestational days (GD) 7-16. The possible protective role of taurine (TA), administered throughout the gestation period (GD 1-20) against Pb toxicity, was also evaluated. Pregnant rats were divided into four groups: Group 1 (control) was given distilled water;Group 2 was exposed to Pb (250 ppm) in drinking water (GD 7-16), whereas Group 3 received TA (50 mg/kg/day) by oral gavage (GD 1-20);Group 4 was exposed to Pb (GD 7-16), whereas pretreated with TA from GD 1 till the end of the gestation period. After termination on GD 20, maternal and embryo-fetal outcomes were evaluated. Blood samples were collected for hematological and biochemical parameters assessment. The results showed that, Pb induced a significant reduction in the maternal body weight, weight gain, uterine and placental weight, in addition to a high incidence of abortion and fetal resorption. Meanwhile, fetuses demonstrated decreased body weight and length, with a high rate of mortality as well as external and skeletal abnormalities. Additionally, Pb induced severe hematological and biochemical alterations in both dams and fetuses. The toxicity of Pb was further emphasized by placental histopathological examination and hepatic DNA fragmentation. Pretreatment with TA greatly attenuated the impact of Pb on both maternal and fetal parameters. Moreover, TA alleviated the incidence of placental damage and hepatic DNA fragmentation. The results highlight the potential prophylaxis role of TA against maternal and developmental Pb toxicity.

Taurine/Pilocarpine Interaction in the Malnourished Rat Brain: A Behavioral, Electrophysiological, and Immunohistochemical Analysis.

This study aimed to evaluate the possible protective role of taurine on anxiety-like behavior, brain electrical activity and glial cell immunoreactivity in well-nourished and malnourished rats that were treated with a subconvulsing dose of pilocarpine. Newborn Wistar rats were subjected to normal or unfavorable lactation conditions, represented by the suckling of litters with 9 or 15 pups, resulting in well-nourished and malnourished animals, respectively. Each nutritional group was split into five subgroups that were treated from postnatal day (PND) 35 to 55 with 300 mg/kg/day of taurine + 45 mg/kg/day of pilocarpine (group T + P), taurine only (group T), pilocarpine only (group P), vehicle control (group V), or not treated control (group naïve; Nv). At PND56-58, the groups were subjected to the elevated plus-maze behavioral tests. Glycemia was measured on PND59. Between PND60 and PND65, the cortical spreading depression (CSD) was recorded in the cerebral cortex, and the levels of malondialdehyde and microglial and astrocyte immunoreactivity were evaluated in the cortex and hippocampus. Our data indicate that treatment with taurine and pilocarpine resulted in anxiolytic-like and anxiogenic behavior, respectively, and that nutritional deficiency modulated these effects. Both treatments decelerated CSD propagation and modulated GFAP- and Iba1-containing glial cells. Pilocarpine reduced body weight and glycemia, and administration of taurine was not able to attenuate the effects of pilocarpine. The molecular mechanisms underlying taurine action on behavioral and electrophysiological parameters in the normal and altered brain remain to be further explored.

Effects of Anabolic Steroids on the Histological Structure of Renal Cortex of Adult Male Albino Rats and the Possible Protective Role of Taurine

Introduction: Misuse of anabolic androgenic steroids (AAS) has become a widespread health problem with subsequent multisystem adverse effects. However, among their adverse effects, renal toxicity remains one of the least discussed.Aim of work: To study the histopathological effects of Nandrolone Decanoate (ND) abuse on renal cortex and examine the possible protective role of taurine. Materials and methods: Thirty-six adult male albino rats, aging 4-6 months and weighing 200 - 250 gms, were used in this study. Animals were divided equally into three groups; Group I (control group): subdivided into Subgroup IA: negative control and Subgroup IB: rats received intramuscular 0.5ml sesame oil twice weekly for six weeks and Subgroup IC: received 100 mg/kg/day Taurine by gavage, for six weeks. Group II (ND Group): received intramuscular 5 mg/kg ND, dissolved in sesame oil, twice weekly for six weeks. Group III (Taurine and ND Group): given both Taurine and ND in the same dose and duration as subgroup IC and group II respectively. At the end of the experiment, venous blood samples were collected from the tail vein for biochemical assays. Kidneys were dissected out and processed for light and electron microscopic examination. Results: Examination of group II revealed marked congestion, obliteration of Bowman’s space and lumina of both proximal and distal tubules. Ultrastructural distortion was evident in glomerular filtration barrier and tubular lining cells. Statistically significant biochemical changes were also observed. However, group III showed almost preserved glomerular and tubular architecture with few persistent changes. Biochemical results also revealed marked improvement. Conclusion: Marked renal cortical affection with renal functional deterioration were noted following ND. Taurine exerted marked reno-protection thus, it would be also of great help to protect AAS users against possible renal hazards in case their AAS use was inevitable.

Bisphenol A-Induced Histopathological Alterations on Small Intestine Tissues of Rats: The Protective Role of Taurine and Curcumin

Bisfenol A (BPA) endokrin bozucu özelliğe sahip bir kimyasaldır. Bu çalışmanın amacı, BPA’nın sıçanince bağırsak dokusunda meydana getirdiği toksik etkiye karşı taurin ve kurkuminin olası koruyucu etkilerini incelemektir.Bu amaçla, kırk iki erkek albino sıçan yedi eşit gruba ayrılmıştır bunlar: kontrol, yağ, taurin(100 mgkg-1 vücut ağırlığı), kurkumin(100 mg kg-1 vücut ağırlığı), bisfenol A (130 mg kg-1 vücut ağırlığı), BPA+taurin veBPA+kurkumin. Uygulamadan dört hafta sonra ince bağırsak dokuları histopatolojik incelemeler için alınmıştır.BPA ince bağırsak dokusunda önemli histopatolojik değişimlere sebep olmuştur, taurin ve kurkumin ise tamamenkoruyucu etki oluşturmamıştır.

Taurine prevents ultraviolet B induced apoptosis in retinal ganglion cells

Background: Compatible osmolytes accumulation is an active resistance response in retina under ultraviolet (UV) radiation and hypertonicity conditions.Objective: The purpose of this research is to investigate the protective role of taurine on retina under UVB radiation.Methods: Osmolytes transporters were measured by quantitative realtime PCR. Osmolytes uptake was estimated by radioimmunoassay. Cell viability was calculated by MTT assay. Cell apoptosis was measured by flow cytometry analysis.Results: Hypertonicity accelerated osmolytes uptake into retinal ganglion cells (RGCs) including taurine, betadine, and myoinositol. UVB radiation increased osmolytes transporter expression and osmolytes uptake. In addition, osmolyte taurine remarkably prevented UVB radiation induced cell apoptosis in RGCs.Conclusions: The effect of compatible osmolyte taurine on cell survival rate may play an important role in cell resistance and adaption to UVB exposure.

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 role of taurine in adaptation of visceral systems under psycho-emotional stress in rats

In the recent years, an identification of regulatory mechanisms underlying the general adaptation syndrome as an organism’s response to drastic emotional stress-evoking environmental changes is gaining in its importance. The ability to control over visceral functions plays a crucial role in stress reactions due to a threat of neurodynamic imbalance in sympathetic-parasympathetic relationships with the heart as their most vulnerable element. Fast stress adaptation promotes restoration not only of the sympathetic-parasympathetic balance, but also of energy metabolism. Taurine is one of the major regulatory molecules that activate metabolic processes. The present work addresses the following issues: (1) the descending influence of the paraventricular nucleus (PVN) on neural reaction of the solitary tract nucleus (STN), which is the first link in the visceral sensitivity pathway, (2) the mechanisms of central control over visceral reactions as investigated by mathematical modelling and analysis of the heart rate variability (HRV), and (3) morphofunctional changes in brain structures, integrating and regulating the visceral sphere (hypothalamic PVN, amygdala), under psycho-emotional stress with and without intraperitoneal injection of taurine (50 mg/kg). Acute and semichronic experiments were conducted on white nonlinear rats under 5-h immobilization stress. An extremely strong centralization of the vegetative HRV parameters (HR, VBI, SSTI) was revealed, with these parameters normalized on days 7 and 14 post taurine injection. An interaction and interdependence of the central regulatory mechanisms of cardiovascular reactions as well as a considerable protective role of taurine, promoting fast restoration of adaptive properties of the central and peripheral visceral sensitivity components under the development of long-term psycho-emotional stress, were shown.

Taurine Attenuates As2O3-Induced Autophagy in Cerebrum of Mouse Through Nrf2 Pathway.

We previously reported that the impairment of cerebrum may relate with neurotoxicity induced by arsenic (As) exposure. In the present study, we investigated whether autophagy of the cerebrum neurons were responsible for As-induced neurotoxicity and the protective role of taurine (Tau). Forty mice were randomly divided into control group, Tau control group, As exposure group and Tau protection group. The results showed that LC3 II expression was elevated and P62 expression was lower after As exposure, whereas the effects were obviously attenuated by Tau treatment. More important, As induced increase of MDA level and decrease of Nrf2 expression were significantly inversed in protective group. In sum, autophagy inhibition might play a strong role in the neuroprotection of Tau in As-induced toxicity via Nrf2 pathway.

Sulfasalazine-induced renal and hepatic injury in rats and the protective role of taurine.

Introduction: Sulfasalazine is a drug commonly administrated against inflammatory-based disorders. On the other hand, kidney and liver injury are serious adverse events accompanied by sulfasalazine administration. No specific therapeutic option is available against this complication. The current investigation was designed to evaluate the potential protective effects of taurine against sulfasalazine-induced kidney and liver injury in rats. Methods: Male Sprague-Dawley rats were administered with sulfasalazine (600 mg/kg, oral) for 14 consecutive days. Animals received different doses of taurine (250, 500 and 1000 mg/ kg, i.p.) every day. Markers of organ injury were evaluated on day 15th, 24 h after the last dose of sulfasalazine. Results: Sulfasalazine caused renal and hepatic injury as judged by an increase in serum level of creatinine (Cr), alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH), and alkaline phosphatase (ALP). The levels of reactive oxygen species (ROS) and lipid peroxidation were raised in kidney and liver of sulfasalazine-treated animals. Moreover, tissue glutathione reservoirs were depleted after sulfasalazine administration. Histopathological changes of kidney and liver also endorsed organ injury. Taurine administration (250, 500 and 1000 mg/kg/day, i.p) alleviated sulfasalazine-induced renal and hepatic damage. Conclusion: Taurine administration could serve as a potential protective agent with therapeutic capabilities against sulfasalazine adverse effects.

Sulfasalazine-Induced Hepatic Injury in an Ex Vivo Model of Isolated Perfused Rat Liver and the Protective Role of Taurine

Sulfasalazine is one of the most commonly administered drugs for the treatment of rheumatoid arthritis and inflammatory bowel disease in humans. On the other hand, acute liver failure led to liver transplantation and/or patient death might occur after sulfasalazine administration. There is no precise mechanism for hepatic injury induced by sulfasalazine and no specific hepatoprotective agent has been developed against this complication. Current investigation was designed to study oxidative stress as a proposed mechanism for sulfasalazine-induced liver injury and evaluate the role of taurine administration as a safe hepatoprotective agent. Methods: Rat liver was isolated after cannulation through portal vein and perfused with Krebs-Henseleit buffer. The liver was exposed to different concentrations of sulfasalazine and taurine. Results: Sulfasalazine (5 mM) administration caused significant hepatic injury as judged by elevation in liver perfusate level of LDH, AST, ALT, and potassium ion (K+). Significant amounts of reactive oxygen species (ROS) and lipid peroxidation were detected in sulfasalazine treated livers. Furthermore, hepatic glutathione reservoirs were depleted. Histopathological examination of liver tissues confirmed the above mentioned biochemical data. Co-administration of taurine (5, 10 and 20 mM), significantly mitigated sulfasalazine-induced hepatic injury in isolated rat liver. Conclusion: The data obtained from current investigation indicate potential therapeutic properties of taurine against sulfasalazine-induced liver injury.

Alteration in estrous cycle, lipid peroxidation and antioxidant status in female rat after exposure to lambda cyhalothrin and its attenuation by taurine

Lambda cyhalothrin, a broad spectrum pyrethroid, is being extensively used against a wide range of pests in agricultural practices. The present study was highlighted to investigate the effects of the lambda cyhalothrin on estrous cycle and oxidative stress in rat ovary, also to find out the protective role of taurine against lambda cyhalothrin induced ovarian toxicity. Mature 36 female Wistar rats were divided in six groups and they were received oral administration of lambda cyhalothrin at two dose levels (8.33 and 16.66 mg/kg body wt) for consecutive14 days. Taurine (50mg/kg body wt) was treated before lambda cyhalothrin administration in the combined taurine-lambda cyhalothrin treated groups. Lambda cyhalothrin caused significant alterations in estrous cycle with an increase in diestrous index compared to control rats. Lambda cyhalothrin treatment also produced oxidative stress in ovary by significant increase in malondialdehyde level, accompanied by a reduction in reduced glutathione and antioxidant enzymes (superoxide dismutase, catalase, glutathione-s-transferase, glutathione peroxidase, glutathione reductase). The present study revealed that the pretreatment of taurine was able to ameliorate lambda cyhalothrin induced ovarian oxidative stress.

Propylthiouracil-Induced Liver Injury in Mice and the Protective Role of Taurine

Propylthiouracil (PTU) is a thionamide drug used in the management of hyperthyroidism in human. On the other hands, several cases of hepatotoxicity, hepatic failure and even death have been reported after PTU administration. No specific protective agent has been developed against this complication yet. Taurine is a sulfur containing amino acid which its beneficial effects in liver tissue has been reported in previous studies. This study was designed to investigate the effect of taurine on PTU‑induced liver injury. Methods: Mice received PTU (100 mg/kg, oral) and different doses of taurine (250, 500 and 1000 mg/kg, i.p, administered 2 hours after PTU) and markers of liver injury were monitored. Results: Acute exposure to PTU caused hepatotoxicity in mice as evidenced by increase in plasmatic alanine aminotransferase (ALT), occurrence of significant lipid peroxidation, and hepatic glutathione depletion. The mentioned changes were endorsed by histopathological lesions of liver which were mainly manifested as pre-portal inflammation. Taurine administration (500 and 1000 mg/kg, i.p) resulted in reduction of lipid peroxidation, showed rebalancing effect on liver GSH level, and normalized plasma ALT. Taurine administration didn’t affect PTU-induced inflammatory cell aggregation in liver. Conclusion: In view of these results, taurine seems to exert some beneficial effects against PTU‑induced liver injury.

Cardiorenal protective effect of taurine against cyclophosphamide-induced toxicity in albino rats.

Cyclophosphamide (CP) is a cytotoxic alkylating agent used in the treatment of malignant diseases and autoimmune disorders. Its clinical use is limited to its marked cardiorenal toxicity. The present study aimed to investigate the possible protective role of taurine (Tau; 200 mg·kg-1 per day, i.p.) on CP-induced cardiorenal toxicity. CP (200 mg·kg-1) was administered as a single intraperitoneal injection whereas; Tau was administered for 3 weeks on a daily basis. The results showed that CP produced an elevation in serum activities of creatine kinase, creatine kinase isoenzyme, lactate dehydrogenase, creatinine as well as blood urea nitrogen. CP also induced an elevation in the oxidative stress markers viz. elevation in the serum lipid peroxides level (measured as malondialdehyde; MDA) and reduction in reduced glutathione level and superoxide dismutase activity in both heart and renal tissue. On the other hand, administration of Tau attenuated the CP-evoked disturbances in the above mentioned parameters. In addition, CP exhibited electrocardiographic (ECG) changes, which were significantly reversed by Tau treatment. Finally, the histopathological examination emphasized the obtained results. In conclusion, Tau is suggested to be a potential candidate to ameliorate CP-induced cardiorenal toxicity that may be related to its antioxidant activity.

Protective role of taurine in developing offspring affected by maternal alcohol consumption.

Maternal alcohol consumption is known to affect offspring growth and development, including growth deficits, physical anomalies, impaired brain functions and behavioral disturbances. Taurine, a sulfur-containing amino acid, is essential during development, and continually found to be protective against neurotoxicity and various tissue damages including those from alcohol exposure. However, it is still unknown whether taurine can exert its protection during development of central nervous system and whether it can reverse alcohol damages on developed brain later in life. This study aims to investigate protective roles of taurine against maternal alcohol consumption on growth and development of offspring. The experimental protocol was conducted using ICR-outbred pregnant mice given 10 % alcohol, with or without maternal taurine supplementation during gestation and lactation. Pregnancy outcomes, offspring mortality and successive bodyweight until adult were monitored. Adult offspring is supplemented taurine to verify its ability to reverse damages on learning and memory through a water maze task performance. Our results demonstrate that offspring of maternal alcohol exposure, together with maternal taurine supplementation show conserved learning and memory, while that of offspring treated taurine later in life are disturbed. Taurine provides neuroprotective effects and preserves learning and memory processes when given together with maternal alcohol consumption, but not shown such effects when given exclusively in offspring.

A pilot study of the onset of hepatic encephalopathy (OHE) in mice induced by thioacetamide and the protective effect of taurine by holistic metabolic characterization

Hepatic encephalopathy (HE) is a severe neuropsychiatric complication due to acute or chronic liver failure. In this work, an acute thioacetamide induced HE mice model was established to investigate the metabolic events in the onset of HE (OHE) and the protective role of taurine (TAU). Sera for biochemical evaluation, and livers and cortexes for histopathological inspection and NMR-based metabolomic investigation were collected. Principal component analysis and orthogonal partial least squares-discriminant analysis were performed to excavate differential metabolites of OHE, and explore the protective role of TAU. Metabolites pathway analysis was performed on significant metabolites selected based on loading/S-plots and fold change plots to identify biologically meaningful metabolic patterns and relevant pathways. The most affected pathways in OHE mice were those along the liver–brain axis: among them, the alanine, aspartate and glutamate metabolism was the most important. TAU showed better performance in improving the disturbed metabolism in the cortex than in the liver of OHE mice. This pilot study based on metabolomics approach and pathway analysis should help to understand HE systematically, and to develop new therapy for HE.