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Taurohyodeoxycholic Acid (sodium salt) Sale

(Synonyms: 牛磺猪去氧胆酸钠) 目录号 : GC48131

A taurine-conjugated form of hyodeoxycholic acid

Taurohyodeoxycholic Acid (sodium salt) Chemical Structure

Cas No.:38411-85-7

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5 mg
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产品描述

Taurohyodeoxycholic acid (THDCA) is a taurine-conjugated form of the secondary bile acid hyodeoxycholic acid .1 THDCA decreases the size and weight of human gallstones in vitro. It increases bile flow, biliary cholesterol secretion, and biliary lipid secretion in rats.2 Co-administration of THDCA with taurochenodeoxycholic acid prevents TCDCA-induced hepatotoxicity, increasing bile flow as well as biliary acid and phospholipid secretion in rats.3 THDCA also reduces myeloperoxidase activity, expression of TNF-α and IL-6, and colonic damage in a mouse model of TNBS-induced ulcerative colitis.4

1.Angelico, M., Mogavero, L., Baiocchi, L., et al.Dissolution of human cholesterol gallstones in bile salt/lecithin mixtures: effect of bile salt hydrophobicity and various pHsScand. J. Gastroenterol.30(12)1178-1185(1995) 2.Angelico, M., Baiocchi, L., Nistri, A., et al.Effect of taurohyodeoxycholic acid, a hydrophilic bile salt, on bile salt and biliary lipid secretion in the ratDig. Dis. Sci.39(11)2389-2397(1994) 3.Roda, A., Piazza, F., Baraldini, M., et al.Taurohyodeoxycholic acid protects against taurochenodeoxycholic acid-induced cholestasis in the ratHepatology27(2)520-525(1998) 4.He, J., Liang, J., Zhu, S., et al.Protective effect of taurohyodeoxycholic acid from Pulvis Fellis Suis on trinitrobenzene sulfonic acid induced ulcerative colitis in miceEur. J. Pharmacol.670(1)229-235(2011)

Chemical Properties

Cas No. 38411-85-7 SDF
别名 牛磺猪去氧胆酸钠
Canonical SMILES C[C@H](CCC(NCCS([O-])(=O)=O)=O)[C@@]1([H])CC[C@@]2([H])[C@]3([H])C[C@H](O)[C@]4([H])C[C@H](O)CC[C@]4(C)[C@@]3([H])CC[C@@]21C.[Na+]
分子式 C26H44NO6S.Na 分子量 521.7
溶解度 DMF: 30 mg/ml,DMF:PBS(pH 7.2)(1:1): 0.5 mg/ml,DMSO: 20 mg/ml,Ethanol: 20 mg/ml 储存条件 Store at -20°C
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1 mM 1.9168 mL 9.5841 mL 19.1681 mL
5 mM 0.3834 mL 1.9168 mL 3.8336 mL
10 mM 0.1917 mL 0.9584 mL 1.9168 mL
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Research Update

Probiotic or synbiotic alters the gut microbiota and metabolism in a randomised controlled trial of weight management in overweight adults

Benef Microbes 2019 Mar 13;10(2):121-135.PMID:30525950DOI:10.3920/BM2018.0028.

The gut microbiota contributes to host energy metabolism, and altered gut microbiota has been associated with obesity-related metabolic disorders. We previously reported that a probiotic alone or together with a prebiotic controls body fat mass in healthy overweight or obese individuals in a randomised, double-blind, placebo controlled clinical study (ClinicalTrials.gov NCT01978691). We now aimed to investigate whether changes in the gut microbiota may be associated with the observed clinical benefits. Faecal and plasma samples were obtained from a protocol compliant subset (n=134) of participants from a larger clinical study where participants were randomised (1:1:1:1) into four groups: (1) placebo, 12 g/d microcrystalline cellulose; (2) Litesse® Ultra™ polydextrose (LU), 12 g/day; (3) Bifidobacterium animalis subsp. lactis 420™ (B420), 1010 cfu/d in 12 g microcrystalline cellulose; (4) LU+B420, 1010 cfu/d of B420 in 12 g/d LU for 6 months of intervention. The faecal microbiota composition and metabolites were assessed as exploratory outcomes at baseline, 2, 4, 6 months, and +1 month post-intervention and correlated to obesity-related clinical outcomes. Lactobacillus and Akkermansia were more abundant with B420 at the end of the intervention. LU+B420 increased Akkermansia, Christensenellaceae and Methanobrevibacter, while Paraprevotella was reduced. Christensenellaceae was consistently increased in the LU and LU+B420 groups across the intervention time points, and correlated negatively to waist-hip ratio and energy intake at baseline, and waist-area body fat mass after 6 months treatment with LU+B420. Functional metagenome predictions indicated alterations in pathways related to cellular processes and metabolism. Plasma bile acids glycocholic acid, glycoursodeoxycholic acid, and Taurohyodeoxycholic Acid and tauroursodeoxycholic acid were reduced in LU+B420 compared to Placebo. Consumption of B420 and its combination with LU resulted in alterations of the gut microbiota and its metabolism, and may support improved gut barrier function and obesity-related markers.

Effect of Taurohyodeoxycholic Acid, a hydrophilic bile salt, on bile salt and biliary lipid secretion in the rat

Dig Dis Sci 1994 Nov;39(11):2389-97.PMID:7956608DOI:10.1007/BF02087656.

Taurohyodeoxycholic Acid is a natural 6 alpha-hydroxylated bile acid with an apparent hydrophilicity intermediate between those of tauroursodeoxycholic and taurocholic acids. We investigated in the rat the hepatobiliary metabolism, choleretic properties, and biliary maximum secretory rate (SRmax) of taurohyodeoxycholic in comparison with these two bile salts. Each compound was infused intravenously, at a rate increased in a stepwise manner from 100 to 300 nmol/min/100 g body wt, in bile salt-depleted bile fistula rats. The three bile salts appeared rapidly starting with the infusion and increased to represent more than 95% of the total bile salts. No apparent biliary metabolites were formed. All the bile salts caused a dose-dependent increase in bile flow and biliary lipid output. The absolute increase in bile flow was lower in rats infused with Taurohyodeoxycholic Acid, yet the volume of bile formed per nanomole of secreted bile salt was 13.8 nl for taurohyodeoxycholic, 6.4 nl for tauroursodeoxycholic acid, and 10.9 nl for taurocholic. The SRmax values were 1080, 3240, and 960 nmol/min/100 g, respectively. At all infusion rates, Taurohyodeoxycholic Acid caused a greater (P < 0.001) secretion of biliary lecithin compared to the other bile salts. There were no significant differences in the biliary secretion of cholesterol and proteins. Electron microscopy showed the recruitment of vesicles and lamellar bodies around and within bile canaliculi. In conclusion, taurohyodeoxycholic promotes a biliary lecithin secretion greater than expected from physicochemical predictions, representing a novel secretory property with potential pharmacological relevance.

Effect of Taurohyodeoxycholic Acid on biliary lipid secretion in humans

Hepatology 1997 Jun;25(6):1306-14.PMID:9185744DOI:10.1002/hep.510250601.

This study aimed to determine the effect in humans of Taurohyodeoxycholic Acid, a 6alpha-hydroxylated bile acid with hydrophilic properties, on bile lipid secretion. Four cholecystectomized patients who had gallstones and an interrupted enterohepatic circulation were intraduodenally infused with taurohyodeoxycholic and tauroursodeoxycholic acids on separate occasions at a dose of 0.8 to 1 g/h for 3 hours. In hourly bile samples collected for 8 hours after the beginning of the infusion, biliary bile acid composition (by high-performance liquid chromatography), biliary lipid concentrations (by standard methods), and distribution of biliary carriers (by gel chromatography) were evaluated. Blood liver function tests were performed before and after the infusions. Taurohyodeoxycholic and tauroursodeoxycholic acids became the predominant biliary bile acids in all patients except for one infused with Taurohyodeoxycholic Acid. Taurohyodeoxycholic Acid stimulated significantly greater (P < .05) cholesterol and phospholipid secretion per unit of secreted bile acid (0.098 and 0.451 micromol/micromol, respectively) compared with tauroursodeoxycholic acid (0.061 micromol/micromol for cholesterol and 0.275 micromol/micromol for phospholipids). The secretory ratio between phospholipid and cholesterol was significantly higher after infusion of Taurohyodeoxycholic Acid (3.88 micromol/micromol) compared with taroursodeoxycholic acid (3.09 micromol/micromol) (P < .05). Biliary enrichment with Taurohyodeoxycholic Acid was positively related with percent concentration of phospholipids but not with that of cholesterol. The opposite trend was observed in tauroursodeoxycholic acid-enriched biles. In both taurohyodeoxycholic acid- and tauroursodeoxycholic acid-rich bile, 80% to 90% of cholesterol was carried in a gel-chromatographic fraction corresponding to an apparent molecular weight of 80 to 200 kd. No alteration in liver function test results was observed after Taurohyodeoxycholic Acid infusion. In conclusion, Taurohyodeoxycholic Acid stimulates greater cholesterol and phospholipid secretion than tauroursodeoxycholic acid, but with a higher phospholipid/cholesterol secretory ratio. In bile enriched with both bile acids, biliary cholesterol is transported in non-micellar aggregates. Finally, in the conditions of our study, Taurohyodeoxycholic Acid was not hepatotoxic.

Taurohyodeoxycholic Acid protects against taurochenodeoxycholic acid-induced cholestasis in the rat

Hepatology 1998 Feb;27(2):520-5.PMID:9462652DOI:10.1002/hep.510270228.

The prevention of the hepatotoxic effects produced by intravenous infusion of taurochenodeoxycholic acid (TCDCA) by coinfusion with Taurohyodeoxycholic Acid (THDCA) was evaluated in bile fistula rats; the hepatoprotective effects of the latter were also compared with those of tauroursodeoxycholic acid (TUDCA). Rats infused with TCDCA at a dose of 8 micromol/min/kg showed reduced bile flow and calcium secretion, as well as increased biliary release of alkaline phosphatase (AP) and lactate dehydrogenase (LDH). This was associated with a very low biliary secretion rate of TCDCA (approximately 1 micromol/min/kg). Simultaneous infusion of THDCA or TUDCA at the same dose preserved bile flow and almost totally abolished the pathological leakage of the two enzymes into bile. The effect was slightly more potent for THDCA. The maximum secretion rate of TCDCA increased to the highest value (8 micromol/min/kg) when coinfused with either of the two hepatoprotective bile acids (BA), which were efficiently and completely secreted in the bile, without metabolism. Calcium output was also restored and phospholipid (PL) secretion increased with respect to the control saline infusion. This increase was higher in the THDCA study. These data show that THDCA is highly effective in the prevention of hepatotoxicity induced by intravenous infusion of TCDCA by facilitating its biliary secretion and reducing its hepatic residence time; this was associated with selective stimulation of PL biliary secretion.

Taurohyodeoxycholic Acid alleviates trinitrobenzene sulfonic acid induced ulcerative colitis via regulating Th1/Th2 and Th17/Treg cells balance

Life Sci 2023 Apr 1;318:121501.PMID:36801213DOI:10.1016/j.lfs.2023.121501.

Aims: Taurohyodeoxycholic Acid (THDCA), a natural 6α-hydroxylated bile acid, exhibits intestinal anti-inflammatory effects. This study aimed to explore the efficacy of THDCA on ulcerative colitis and to reveal its mechanisms of action. Main methods: Colitis was induced by intrarectal administration of trinitrobenzene sulfonic acid (TNBS) to mice. Mice in the treatment group were gavage THDCA (20, 40, and 80 mg/kg/day) or sulfasalazine (500 mg/kg/day) or azathioprine (10 mg/kg/day). The pathologic markers of colitis were comprehensively assessed. The levels of Th1-/Th2-/Th17-/Treg-related inflammatory cytokines and transcription factors were detected by ELISA, RT-PCR, and Western blotting. The balance of Th1/Th2 and Th17/Treg cells was analyzed by Flow cytometry. Key findings: THDCA significantly alleviated colitis by improving the body weight, colon length, spleen weight, histological characteristics, and MPO activity of colitis mice. THDCA reduced the secretion of Th1-/Th17-related cytokines (IFN-γ, IL-12p70, IL-6, IL-17A, IL-21, IL-22, and TNF-α) and the expressions of transcription factors (T-bet, STAT4, RORγt, and STAT3), but increase the production of Th2-/Treg-related cytokines (IL-4, IL-10, and TGF-β1) and the expressions of transcription factors (GATA3, STAT6, Foxp3, and Smad3) in the colon. Meanwhile, THDCA inhibited the expressions of IFN-γ, IL-17A, T-bet, and RORγt, but improved the expression of IL-4, IL-10, GATA3, and Foxp3 in the spleen. Furthermore, THDCA restored the proportion of Th1, Th2, Th17, and Treg cells, and balanced the Th1/Th2 and Th17/Treg immune response of colitis mice. Significance: THDCA can alleviate TNBS-induced colitis via regulating Th1/Th2 and Th17/Treg balance, which may represent a promising treatment for patients with colitis.