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Tauroursodeoxycholic acid

Q: What are the different forms or variations of Tauroursodeoxycholic acid?

Tauroursodeoxycholic acid (TUDCA) is a naturally occurring bile acid that can exist in different forms or chemical variations. The most common form is the sodium salt, which is often used in research and clinical applications. However, TUDCA can also be found in free acid form or other salt forms, such as the calcium or potassium salts. The specific form used may depend on the intended application and formulation requirements.

Q: What are the key therapeutic applications of Tauroursodeoxycholic acid?

Tauroursodeoxycholic acid (TUDCA) has been studied for its potential therapeutic benefits in a variety of conditions, including: 1. Liver disorders: TUDCA has been investigated for its use in treating liver diseases, such as primary biliary cholangitis, non-alcoholic fatty liver disease, and alcoholic liver disease, due to its cytoprotective and anti-inflammatory properties. 2. Gastrointestinal disorders: TUDCA may have beneficial effects in managing gastrointestinal conditions, including inflammatory bowel diseases and peptic ulcers, by modulating bile acid metabolism and reducing inflammation. 3. Neurological disorders: Research suggests that TUDCA may have neuroprotective effects and could be potentially useful in the management of neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and Huntington's disease.

Q: How can PubCompare.ai assist with Tauroursodeoxycholic acid research?

PubCompare.ai can be a valuable tool for researchers studying Tauroursodeoxycholic acid (TUDCA) in the following ways: 1. Efficient protocol screening: The platform allows you to quickly and easily search through a vast database of protocols from literature, preprints, and patents related to TUDCA research, saving you time and effort. 2. AI-driven protocol comparisons: PubCompare.ai's AI-powered analysis can help you identify the most effective and reproducible protocols for your specific research goals by highlighting key differences in protocol effectiveness. 3. Improved accuracy and reproducibility: By leveraging the insights provided by PubCompare.ai, you can make more informed decisions about which TUDCA protocols to use, leading to greater accuracy and reproducibility in your research.

Q: Are there any common challenges or considerations in using Tauroursodeoxycholic acid for research or therapeutic purposes?

When using Tauroursodeoxycholic acid (TUDCA) for research or therapeutic applications, there are a few key considerations to keep in mind: 1. Solubility: TUDCA has limited solubility in aqueous solutions, which can pose challenges in formulating and administering it effectively. Researchers may need to explore different solvents or delivery methods to overcome this issue. 2. Stability: TUDCA can be sensitive to environmental factors, such as temperature, pH, and light exposure. Proper storage and handling conditions are important to maintain the stability and potency of TUDCA samples. 3. Dosage optimization: The optimal dosage of TUDCA may vary depending on the specific application and target population. Researchers and clinicians may need to carefully titrate the dose to achieve the desired therapeutic effects while minimizing potential side effects.

Tauroursodeoxycholic acid is a bile acid found naturally in the human body.
It plays a role in bile acid metabolism and has been studied for its potential therapeutic applications, including in liver and gastrointestinal disorders.
PubCompare.ai can help researchers easily locate relevant protocols from literature, preprints, and patents, and leverage AI-driven comparisons to identify the best methods and products for Tauroursodeoxycholic acid research.
This can improve reproducibility and accuracy, enhancing your understanding of this important bile acid.

Most cited protocols related to «Tauroursodeoxycholic acid»

Synthetic Aβ Homologue Preparation and Aggregation

Cited 6 times

Synthetic Aβ homologues were dissolved to 1 mM in hexafluoro-isopropanol (HFIP; Sigma Chemical Co., St. Louis, MO), a pre-treatment that breaks down β-sheet structures and disrupts hydrophobic forces leading to monodisperse Aβ preparations [34 (link)]. Following lyophilization to remove HFIP, peptides were subsequently solubilized in deionized water and added to an equal volume of a 2× concentrated phosphate-buffered saline (PBS), pH 7.4, to a final concentration of 1 mg/ml in 1 × PBS. Peptides, in the presence or absence of 100 µM TUDCA (Sigma), were either incubated at 37°C for up to 48 h for the aggregation studies or diluted into culture media at the required concentration for the toxicity experiments. For the aggregation studies, structural properties were assessed by Western blot analysis, circular dichroism (CD) spectroscopy and Thioflavin T binding.

Viana R.J., Nunes A.F., Castro R.E., Ramalho R.M., Meyerson J., Fossati S., Ghiso J., Rostagno A, & Rodrigues C.M. (2009). Tauroursodeoxycholic acid prevents E22Q Alzheimer’s Aβ toxicity in human cerebral endothelial cells. Cellular and molecular life sciences : CMLS, 66(6), 1094-1104.

Publication 2009

Circular Dichroism Culture Media Freeze Drying Isopropyl Alcohol Peptides Phosphates Saline Solution Spectrum Analysis tauroursodeoxycholic acid thioflavin T Western Blot

Murine Cardiomyocyte Isolation and Oxidative Stress

Cited 4 times

Protocol full text hidden due to copyright restrictions

Open the protocol to access the free full text link

Publication 2009

Acetylcysteine Antioxidants Cells diacetylmonoxime Glucose Heart HEPES isolation Ketamine Left Ventricles Liberase Magnesium Chloride Mus Muscle Cells Muscle Contraction Myocytes, Cardiac Oxidative Stress Sarcomeres Sedatives Sodium Chloride tauroursodeoxycholic acid Tissues Vitamin K3 Xylazine

Evaluating Mitochondrial Dysfunction and Cybrids

Cited 4 times

Unless otherwise stated, human ND1-mutant (3796A>G) cybrid, human MELAS (A3243G-Leucine tRNA) cybrid, human LHON ND6 (G14459A) cybrids, and control cybrid cells were routinely cultured in Dulbecco’s modified Eagle’s medium (DMEM) (Gibco) containing 10% fetal bovine serum, 100 U/mL penicillin and streptomycin, 1 mM sodium pyruvate, and 4 mM l-glutamine. Mouse Rieske knockout cells were cultured in the same media, but also supplemented with 5 μg/mL uridine. Depending on the experiment, media also contained either 10 mM galactose or 25 mM glucose. For cell survival experiments: 100,000 cells were seeded directly in galactose-media with or without compounds or in glucose media containing varying dosages of tunicamycin. Cells were trypsinized and counted 48 or 72 h later unless otherwise stated.
Drug treatments included: 25 μM glimepiride unless otherwise stated (Santa Cruz Biotechnology Inc.), 25 μm glyburide (Sigma-Aldrich), 25 μM repaglinide (Sigma-Aldrich), 25 μM SB203580 (Santa Cruz Biotechnology Inc.), 2 μM SB202190 (Sigma-Aldrich), 20 μM SP600125 (Sigma-Aldrich), 1 mM sodium 4-phenylbutyrate, 500 μM Tauroursodeoxycholic acid sodium salt (Fisher Scientific), 100 μM d-(+)-glucosamine (Sigma-Aldrich), 25 μM B I09 (Tocris), 20 μM 4 μ8C (7-hydroxy-4-methyl-2-oxo-2H-chromene-8-carbaldehyde, Sigma), tunicamycin (Sigma-Aldrich) at varying dosages. Drug treatments were typically performed for either 48 or 72 h in galactose media unless otherwise noted.
CRISPR constructs: The lentiCRISPR v2 plasmid (addgene #52961) was used to clone all CRISPR constructs. Guide sequences for Kir6.2 were as follows. Kir6.2#1, 5′-CACCGAAGTGACTATTGGCTTTGGG-3′; Kir6.2#2, 5′-CACCGGAGTGGATGCTGGTGACAC-3′.

Soustek M.S., Balsa E., Barrow J.J., Jedrychowski M., Vogel R., Jan S.m.e.i.t.i.n.k., Gygi S.P, & Puigserver P. (2018). Inhibition of the ER stress IRE1α inflammatory pathway protects against cell death in mitochondrial complex I mutant cells. Cell Death & Disease, 9(6), 658.

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Publication 2018

2H-chromene Cells Cell Survival Clone Cells Clustered Regularly Interspaced Short Palindromic Repeats Culture Media Eagle Fetal Bovine Serum Galactose glimepiride Glucosamine Glucose Glutamine Glyburide Homo sapiens Leucine MELAS Syndrome Mus Optic Atrophy, Hereditary, Leber Penicillins Pharmaceutical Preparations Plasmids Pyruvate repaglinide SB 202190 SB 203580 Sodium Sodium Chloride sodium phenylbutyrate SP600125 Streptomycin tauroursodeoxycholic acid Transfer RNA Tunicamycin Uridine

Retinal Microglial Cell Analysis in Rat Models

Cited 3 times

Morphology, spatial distribution and mean number of microglial cells were analyzed in the inner and outer plexiform layers (IPL, OPL), the ganglion cell layer (GCL) and the subretinal space (SS) of whole-mount retinas. Macrophages detected in the GCL during the analysis were also accounted. Four to six retinas from each animal group (TUDCA-treated, untreated and SD animals) were examined. In each retina, 12 representative regions of 0.227 mm² each were analyzed, 6 regions equidistantly arranged on the superior-inferior axis of the retina and 6 fields disposed on the temporal-nasal axis; thus sampling representative peripheral, medial and central areas of the superior, inferior, temporal and nasal quadrants of each retina. In each of the 12 regions analyzed in each retina, every one of the cell bodies labeled with immunoperoxidase in each of the 3 layers analyzed was manually traced using a camera lucida attached to the Leica DMR microscope (Leica Microsystems, Wetzlar, Germany). Each retinal layer was determined according to the vascular stratification of the retinal tissue. The images created were subsequently digitized using the image-editing software Photoshop (Adobe Systems Inc., San Jose, CA, USA). The distribution pattern of microglial cells in each retinal layer was assessed by measuring the distances to the nearest neighbors of each microglial cell using ImageJ software [39 ]. The distances to the nearest neighbors were classified in histograms, statistically analyzed and compared with a nearest neighbor analysis of a random pattern of the same density and standard deviation [39 ,40 (link)]. For nearest neighbor distance analysis we used images collected from the medial area of the retina (superior quadrant).Figure 1

Distribution and morphology of microglial cells in Sprague-Dawley (SD) (A) and P23H (B) rats. Retinal vertical sections were immunolabeled with CD11b (OX-42). Note the presence of amoeboid CD11b-positive cells in different layers of the P23H rat retina, including the subretinal space. GCL, ganglion cell layer; IPL, inner plexiform layer; INL, inner nuclear layer; OPL, outer plexiform layer; ONL, outer nuclear layer. Scale bar: 10 μm.

Figure 2

Drawing of the most representative morphology and location of microglial cells in Sprague-Dawley (SD) (A), untreated P23H (B) and tauroursodeoxycholic acid (TUDCA)-treated P23H (C) rats. Note the absence of microglial cells into the subretinal space of P23H rats treated with TUDCA. GCL, ganglion cell layer; IPL, inner plexiform layer; INL, inner nuclear layer; OPL, outer plexiform layer; ONL, outer nuclear layer; SS, subretinal space.

Figure 3

Migration of microglia into the subretinal space of untreated P23H rats. Whole-mount retina of a SD (A), untreated P23H (B) and tauroursodeoxycholic acid (TUDCA)-treated P23H (C) rat immunolabeled with CD11b (OX-42), showing the presence of amoeboid microglial cells in the subretinal space of untreated P23H rats. Scale bar: 40 μm.

Figure 4

Quantification of retinal microglial cells. (A) Average number of positively stained microglial cells quantified in whole-mount retinas from SD (n = 4; green), untreated P23H (n = 6; red) and tauroursodeoxycholic acid (TUDCA)-treated P23H rats (n = 6; grey). (B) Average number of microglial cells in the GCL, IPL, OPL and SS of the retinas analyzed in (A). *P <0.05, **P <0.01, ***P <0.001; ANOVA, Bonferroni’s test.

To analyze microglial activation in each animal group, we used cryostat vertical retinal sections immunostained with Iba1 and MHC-II. We examined three vertical sections non-consecutive per animal and we studied six animals per experimental group. All the images analyzed were collected from the central area of the retina, close to the optic nerve. In every retinal section, the total number of microglial cells expressing one or both markers (Iba1⁺/MHC-II⁻, Iba1⁻/MHC-II⁺ and Iba1⁺/MHC-II⁺) was counted using light microscopy at x63 magnification. The obtained data were referred to the length of each retinal section, measured using the ImageJ software.

Noailles A., Fernández-Sánchez L., Lax P, & Cuenca N. (2014). Microglia activation in a model of retinal degeneration and TUDCA neuroprotective effects. Journal of Neuroinflammation, 11, 186.

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Publication 2014

Streptozotocin-Induced Diabetes Protocol

Cited 3 times

Insulinopenia and persistent hyperglycaemia was induced in experimental mice using low dose streptozotocin (STZ, 60 mg/kg, freshly dissolved in 0.05 M sterile sodium citrate, pH 4.5) on five successive days in 8-week-old mice as described5 (link),17 (link),19 . To study the consequences of insulin resistance db/db mice were used. For further details see supplementary information.
Subgroup of mice received various interventions. We intraperitoneally injected either tauroursodeoxycholic acid (TUDCA) (150 mg/kg bodyweight, dissolved in saline) or saline once daily starting 18 weeks after the last streptozotocin (STZ) injection until 1 d before analyses (week 26) in some mice5 (link). In other mice we intraperitoneally injected aPC (1 mg/kg bodyweight, every alternate day) or an equal volume of saline. Aditionally, in a subgroup of mice aPC was pre-incubated before injection with the HAPC¹⁵⁷³ antibody at a 1:1 ratio for 10 min under gentle agitation to block its anticoagulant activity20 (link),21 (link). Human aPC was used throughout the study, which was generated following an established protocol22 (link).

Madhusudhan T., Wang H., Ghosh S., Dong W., Kumar V., Al-Dabet M.M., Manoharan J., Nazir S., Elwakiel A., Bock F., Kohli S., Marquardt A., Sögüt I., Shahzad K., Müller A.J., Esmon C.T., Nawroth P.P., Reiser J., Chavakis T., Ruf W, & Isermann B. (2017). Signal integration at the PI3K-p85-XBP1 hub endows coagulation protease activated protein C with insulin-like function. Blood, 130(12), 1445-1455.

Publication 2017

Anticoagulants Body Weight Cardiac Arrest Homo sapiens Hyperglycemia Immunoglobulins Insulin Resistance Mice, House Saline Solution Sodium Citrate Sterility, Reproductive Streptozocin tauroursodeoxycholic acid

Most recents protocols related to «Tauroursodeoxycholic acid»

Bile Acid Profiling by LC-MS/MS

The bile acid profile was detected using liquid chromatography-tandem mass spectrometry (LC–MS/MS) with the API3200MD triple quadrupole mass spectrometer (ABSciex, USA) and Shimadzu series liquid chromatograph (Shimadzu, Japan). The reagent kits were purchased from Shanghai ClinMeta Co., Ltd. The assay comprised 15 components: cholic acid (CA), glycocholic acid (GCA), taurocholic acid (TCA), chenodeoxycholic acid (CDCA), glycochenodeoxycholic acid (GCDCA), taurochenodeoxycholic acid (TCDCA), deoxycholic acid (DCA), glycodeoxycholic acid (GDCA), taurodeoxycholic acid (TDCA), lithocholic acid (LCA), glycolithocholic acid (GLCA), taurolithocholic acid (TLCA), ursodeoxycholic acid (UDCA), glycoursodeoxycholic acid (GUDCA), and tauroursodeoxycholic acid (TUDCA).

Xu R., Shen J., Song Y., Lu J., Liu Y., Cao Y., Wang Z, & Zhang J. (2024). Exploration of the application potential of serum multi-biomarker model in colorectal cancer screening. Scientific Reports, 14, 10127.

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Publication 2024

Murine Islet Dissociation and Tunicamycin Treatment

Whole islets were isolated from NOD mice as described and dispersed for 3 min at 37°C using non-enzymatic cell dissociation buffer (Millipore Sigma). Cells were collected by centrifugation, washed with PBS, and counted. Cells were resuspended in DMEM/10% FBS low-glucose media (1 g/L glucose, Gibco, D10F-LG) and split into 1.0 mL aliquots in microfuge tubes for treatment overnight at 37°C in D10F-LG or D10F-LG containing 100 µM tauroursodeoxycholic acid (TUDCA; Millipore Sigma). Tunicamycin (Millipore Sigma) was added at 1 µg/mL to appropriate samples and was incubated for 2 h at 37°C, after which cells were collected, washed, and counted for antigen assays.

Wenzlau J.M., Peterson O.J., Vomund A.N., DiLisio J.E., Hohenstein A., Haskins K, & Wan X. (2024). Mapping of a hybrid insulin peptide in the inflamed islet β-cells from NOD mice. Frontiers in Immunology, 15, 1348131.

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Publication 2024

Hepatoprotective Strategies Against Ischemia-Reperfusion Injury

While options for managing IRI in liver diseases are limited, several treatments have emerged that effectively protect hepatocytes. Trimetazidine in the IGL-1 solution inhibits p53 and activates SIRT1, thus protecting hepatocytes from IRI (Pantazi et al., 2015b (link)). Rebamipide reduces inflammation and improves histological alterations in the liver, crucial for recovery post-reperfusion, which increases SIRT1 expression and modulatesβ-catenin and FOXO1, while suppressing NF- κB p65 expression (Gendy, Abdallah & El-Abhar, 2017 (link); Elwany et al., 2023 (link)). Losartan mitigates liver injury associated with transplantation, improving overall transplantation success rates via SIRT1, enhancing the liver’s defense against oxidative stress and inflammation (Pantazi et al., 2015a (link)). Tauroursodeoxycholic acid modulates the SIRT1/FXR signaling pathway beneficial in managing IRI during liver surgeries (Sun et al., 2020 (link)). Pachymic acid maintains SIRT1 expression during oxygen-glucose deprivation/reoxygenation (Xue et al., 2023a (link); Xue et al., 2023b (link)).

Wang M., Zhao J., Chen J., Long T., Xu M., Luo T., Che Q., He Y, & Xu D. (2024). The role of sirtuin1 in liver injury: molecular mechanisms and novel therapeutic target. PeerJ, 12, e17094.

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Publication 2024

Quantification of Plasma Bile Acids

Fasting blood samples were collected from consenting participants at recruitment, separated by components, and stored at -80 °C until measurement. After solvent extraction, plasma samples were detected for BAs in the multiple reaction monitoring mode on a ultraperformance liquid chromatography, coupled to tandem mass spectrometry (UPLC-MS/MS, Agilent Technologies, USA), according to the previously optimized method with minor modifications [26 (link)]. The target BAs included unconjugated primary BAs (cholate [CA] and chenodeoxycholate [CDCA]) and their amino acid conjugates (glycocholate [GCA], taurocholate [TCA], glycochenodeoxycholate [GCDCA], taurochenodeoxycholate [TCDCA]), as well as unconjugated secondary BAs (deoxycholate [DCA], lithocholate [LCA], hyocholic acid [HCA], and ursodeoxycholate [UDCA]) and conjugated secondary BAs (glycodeoxycholate [GDCA], taurodeoxycholate [TDCA], glycolithocholate [GLCA], taurolithocholic acid [TLCA], glycohyocholic acid [GHCA], taurohyocholic acid [THCA], glycoursodeoxycholate [GUDCA] and tauroursodeoxycholic acid [TUDCA]). BAs were quantified by calibration curves constructed from standards and corresponding isotopically labelled internal standards using MassHunter Workstation software (Agilent, Version B.08.00). BAs with detection rates below 80% (except for LCA) were omitted from subsequent analyses. The values below the limits of detection were imputed with the half minimum across all subjects. The intra-assay CVs ranged from 3.6 to 18.6% for all included BAs.

Geng T., Lu Q., Jiang L., Guo K., Yang K., Liao Y.F., He M., Liu G., Tang H, & Pan A. (2024). Circulating concentrations of bile acids and prevalent chronic kidney disease among newly diagnosed type 2 diabetes: a cross-sectional study. Nutrition Journal, 23, 28.

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Publication 2024

Liver Ischemia-Reperfusion Injury Model

As mentioned previously,⁷ (link)¹⁷ (link) a stable mouse model was established using 70% partial hepatic heat IR. Mice were anesthetized and a laparotomy was performed to expose the liver. The left and middle branches of the intrahepatic portal vein were clamped to block the blood supply. The clips were released for reperfusion after 90 minutes of ischemia. The sham mice underwent the same procedure but without clamping the blood vessels. The mice were sacrificed 6 hours after reperfusion, and liver and blood samples were collected for analysis.
To study the effects of ER stress, Control and HFD-fed mice were injected with tauroursodeoxycholic acid (TUDCA) i.p. (400 mg/kg) or PBS (Control) for 3 days, and then the model of liver IR was established.
To determine the role of mitochondrial oxidation, Control and HFD-fed mice were pretreated with the mitochondria-targeted antioxidant Mito-TEMPO (5 mg/kg, MedChemExpress, HY-112879) twice at 17 hours and 1 hour before surgery or PBS.

Li F., Guan Z., Gao Y., Bai Y., Zhan X., Ji X., Xu J., Zhou H, & Rao Z. (2024). ER stress promotes mitochondrial calcium overload and activates the ROS/NLRP3 axis to mediate fatty liver ischemic injury. Hepatology Communications, 8(4), e0399.

Publication 2024

Top products related to «Tauroursodeoxycholic acid»

Tauroursodeoxycholic acid by Merck Group

Sourced in United States, Germany, United Kingdom

Tauroursodeoxycholic acid is a bile acid derivative that is used as a laboratory reagent. It is a white to off-white crystalline powder that is soluble in water and organic solvents. Tauroursodeoxycholic acid is commonly used in biochemical research and assays, but its specific applications are not detailed here.

Tudca by Merck Group

Sourced in United States, United Kingdom, Germany

TUDCA is a bile acid derivative produced by Merck Group. It is a white crystalline powder with a molecular formula of C26H45NO6. TUDCA acts as an osmotic agent and has been observed to have cytoprotective properties.

Ursodeoxycholic acid by Merck Group

Sourced in United States, United Kingdom, Germany, Switzerland

Ursodeoxycholic acid is a chemical compound that is used as a pharmaceutical ingredient in various medical products. It is a naturally occurring bile acid that can be synthesized for use in laboratory and medical applications. The core function of ursodeoxycholic acid is to act as a bile acid and assist in the regulation of bile production and metabolism.

Cholic acid by Merck Group

Sourced in United States, Germany, United Kingdom, Sao Tome and Principe, Switzerland, Canada, Japan, Macao, New Zealand, China

Cholic acid is a natural bile acid found in the human body. It is used as a basic laboratory compound for various research and analytical purposes.

Deoxycholic acid by Merck Group

Sourced in United States, Germany, United Kingdom, Switzerland, Belgium, China, Canada, France

Deoxycholic acid is a bile acid that is commonly used in laboratory settings. It is a white, crystalline powder with a molecular formula of C₂₄H₄₀O₄. Deoxycholic acid functions as a surfactant and is often utilized in various biochemical and cell biology applications.

Taurodeoxycholic acid by Merck Group

Sourced in United States, United Kingdom, Switzerland, Canada, Ireland

Taurodeoxycholic acid is a bile acid compound that is commonly used as a laboratory reagent. It serves as a solubilizing agent and is employed in various biochemical and cell culture applications.

Taurocholic acid by Merck Group

Sourced in United States, United Kingdom, Switzerland, Germany, Sao Tome and Principe

Taurocholic acid is a bile acid that functions as a surfactant, facilitating the digestion and absorption of fats in the small intestine. It is a key component in the bile produced by the liver and plays a role in the emulsification and solubilization of lipids.

Taurochenodeoxycholic acid by Merck Group

Sourced in United States, Germany, United Kingdom, Switzerland

Taurochenodeoxycholic acid is a laboratory reagent used in biochemical research. It is a bile acid derivative that serves as a fundamental component in various analytical and experimental procedures. The core function of taurochenodeoxycholic acid is to facilitate specific chemical reactions and analyses in a controlled laboratory environment, though its precise applications may vary depending on the research context.

Chenodeoxycholic acid by Merck Group

Sourced in United States, Germany, Switzerland, France, United Kingdom, Canada, Belgium

Chenodeoxycholic acid is a naturally occurring bile acid. It is a key component in the biosynthesis of bile salts and is involved in the regulation of cholesterol levels in the body.

Fetal bovine serum (fbs) by Thermo Fisher Scientific

Sourced in United States, China, United Kingdom, Germany, Australia, Japan, Canada, Italy, France, Switzerland, New Zealand, Brazil, Belgium, India, Spain, Israel, Austria, Poland, Ireland, Sweden, Macao, Netherlands, Denmark, Cameroon, Singapore, Portugal, Argentina, Holy See (Vatican City State), Morocco, Uruguay, Mexico, Thailand, Sao Tome and Principe, Hungary, Panama, Hong Kong, Norway, United Arab Emirates, Czechia, Russian Federation, Chile, Moldova, Republic of, Gabon, Palestine, State of, Saudi Arabia, Senegal

Fetal Bovine Serum (FBS) is a cell culture supplement derived from the blood of bovine fetuses. FBS provides a source of proteins, growth factors, and other components that support the growth and maintenance of various cell types in in vitro cell culture applications.

What are the different forms or variations of Tauroursodeoxycholic acid?

Tauroursodeoxycholic acid (TUDCA) is a naturally occurring bile acid that can exist in different forms or chemical variations. The most common form is the sodium salt, which is often used in research and clinical applications. However, TUDCA can also be found in free acid form or other salt forms, such as the calcium or potassium salts. The specific form used may depend on the intended application and formulation requirements.

What are the key therapeutic applications of Tauroursodeoxycholic acid?

Tauroursodeoxycholic acid (TUDCA) has been studied for its potential therapeutic benefits in a variety of conditions, including: 1. Liver disorders: TUDCA has been investigated for its use in treating liver diseases, such as primary biliary cholangitis, non-alcoholic fatty liver disease, and alcoholic liver disease, due to its cytoprotective and anti-inflammatory properties. 2. Gastrointestinal disorders: TUDCA may have beneficial effects in managing gastrointestinal conditions, including inflammatory bowel diseases and peptic ulcers, by modulating bile acid metabolism and reducing inflammation. 3. Neurological disorders: Research suggests that TUDCA may have neuroprotective effects and could be potentially useful in the management of neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and Huntington's disease.

How can PubCompare.ai assist with Tauroursodeoxycholic acid research?

PubCompare.ai can be a valuable tool for researchers studying Tauroursodeoxycholic acid (TUDCA) in the following ways: 1. Efficient protocol screening: The platform allows you to quickly and easily search through a vast database of protocols from literature, preprints, and patents related to TUDCA research, saving you time and effort. 2. AI-driven protocol comparisons: PubCompare.ai's AI-powered analysis can help you identify the most effective and reproducible protocols for your specific research goals by highlighting key differences in protocol effectiveness. 3. Improved accuracy and reproducibility: By leveraging the insights provided by PubCompare.ai, you can make more informed decisions about which TUDCA protocols to use, leading to greater accuracy and reproducibility in your research.

Are there any common challenges or considerations in using Tauroursodeoxycholic acid for research or therapeutic purposes?

When using Tauroursodeoxycholic acid (TUDCA) for research or therapeutic applications, there are a few key considerations to keep in mind: 1. Solubility: TUDCA has limited solubility in aqueous solutions, which can pose challenges in formulating and administering it effectively. Researchers may need to explore different solvents or delivery methods to overcome this issue. 2. Stability: TUDCA can be sensitive to environmental factors, such as temperature, pH, and light exposure. Proper storage and handling conditions are important to maintain the stability and potency of TUDCA samples. 3. Dosage optimization: The optimal dosage of TUDCA may vary depending on the specific application and target population. Researchers and clinicians may need to carefully titrate the dose to achieve the desired therapeutic effects while minimizing potential side effects.

More about "Tauroursodeoxycholic acid"

Tauroursodeoxycholic acid (TUDCA) is a naturally occurring bile acid found in the human body that plays a crucial role in bile acid metabolism.
This important compound has been extensively studied for its potential therapeutic applications, particularly in the management of liver and gastrointestinal disorders.
TUDCA, also known as taurine-conjugated ursodeoxycholic acid, is closely related to ursodeoxycholic acid (UDCA), another bile acid with similar properties.
Both TUDCA and UDCA are considered to be secondary bile acids, meaning they are derived from primary bile acids such as cholic acid and chenodeoxycholic acid.
In addition to its role in bile acid metabolism, TUDCA has been investigated for its potential benefits in a variety of other health conditions, including neurological disorders, metabolic syndromes, and even certain types of cancer.
Researchers have explored the use of TUDCA as a therapeutic agent, as well as its potential synergistic effects when combined with other compounds like fetal bovine serum (FBS).
To enhance the accuracy and reproducibility of TUDCA-related research, scientists can utilize tools like PubCompare.ai to easily locate relevant protocols from the literature, preprints, and patents.
This AI-driven comparison platform can help researchers identify the best methods and products for their TUDCA studies, ultimately improving the overall quality and impact of their work.
Whether you're studying the fundamental biology of TUDCA or exploring its therapeutic potential, a comprehensive understanding of this versatile bile acid and the resources available for conducting high-quality research can be invaluable.
By staying up-to-date with the latest developments in TUDCA research, you can stay ahead of the curve and contribute to the ongoing advancements in this important field of study.