Dehydrolithocholic Acid (Synonyms: 3-keto LCA, 3-keto Lithocholate, 3-keto Lithocholic Acid, 3-KLCA, 3-oxo LCA, 3-oxo Lithocholate, 3-oxo Lithocholic Acid) |
| Catalog No.GC47182 |
Dehydrolithocholic acid (3-Oxo-5β-cholanoic acid; 3-oxoLCA; DLA) is a bile acid metabolite that inhibits T helper cell 17 (Th17) differentiation by interacting with retinoic acid receptor associated orphan receptor (RORγt).
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 1553-56-6
Sample solution is provided at 25 µL, 10mM.
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Dehydrolithocholic acid (3-Oxo-5β-cholanoic acid; 3-oxoLCA; DLA) is a bile acid metabolite that inhibits T helper cell 17 (Th17) differentiation by interacting with retinoic acid receptor associated orphan receptor (RORγt) [1]. Bile acids are natural surfactants derived from cholesterol, which are crucial for lipid digestion and glucose metabolism, protecting the intestinal epithelium and endowing the mammalian gut with resistance to pathogens[2]. Dehydrolithocholic acid can be a potential candidate drug for the treatment of inflammatory bowel disease[1].
In vitro, use Dehydrolithocholic acid (5µM; 24 hours) can activate the TGR 5-ERK 1/2 pathway on the surface of bronchial epithelial cells (HBEpC) and increase the expression of cathelicidin in the cells[3]. Use Dehydrolithicholic Acid (20µM; 48 hours) treatment with primary CD4+T cells can inhibit Th 17 differentiation and reduce IL-17 α expression levels, but does not affect T cell differentiation into Th 1 or Th 2 cells[4]. MKN 45 was cultured in serum-free medium and treated with 10ng/mL LIF alone or in combination with Dehydrolithocholic acid (1, 3, 10, and 20μM) to reverse LIF induced cell growth at the lowest concentration of 1μM[5].
In vivo, Jax-B6 mice were fed with fecal slurry containing SFB (segmented filamentous bacteria from C57 BL/6 NTac mice) and fed with a control diet or a diet containing 0.3% (w/w) Dehydrolithocholic acid for one week. Treatment with Dehydrolithocholic acid significantly reduced the percentage of Th17 cells in the mouse gut[4]. The rat MCAO model was treated with Dehydrolithocholic acid (pre ischemic administration; 10mg/kg; ip.), which significantly promoted neuronal death in primary culture after OGD injury by downregulating PLOD 2 levels and increasing PTEN expression[6].
References:
[1] Hang S, Paik D, Yao L, et al. Bile acid metabolites control T(H)17 and T(reg) cell differentiation[J]. Nature, 2019, 576(7785): 143-148.
[2] Cheng W, Zhou X, Jin C, et al. Acid-base transformative HADLA micelles alleviate colitis by restoring adaptive immunity and gut microbiome[J]. J Control Release, 2023, 364: 283-296.
[3] Iwona T Myszor, Kornelia Lapka, et al. Bile acid metabolites enhance expression of cathelicidin antimicrobial peptide in airway epithelium through activation of the TGR5-ERK1/2 pathway. Sci Rep. 2024 Mar 21;14(1):6750.
[4] Saiyu Hang, Donggi Paik, et al. Bile acid metabolites control Th17 and Treg cell differentiation. Nature. 2019 Dec;576(7785):143-148.
[5] Cristina Di Giorgio, Elva Morretta, et al. Bile acids serve as endogenous antagonists of the Leukemia inhibitory factor (LIF) receptor in oncogenesis. Biochem Pharmacol. 2024 May:223:116134.
[6] Xiangyi Kong, Xujin Yao, et al. tDCS Regulates ASBT-3-OxoLCA-PLOD2-PTEN Signaling Pathway to Confer Neuroprotection Following Rat Cerebral Ischemia-Reperfusion Injury. Mol Neurobiol. 2023 Nov;60(11):6715-6730.
| Cell experiment [1]: | |
Cell lines | Primary CD4+T cells from wild-type B6 mice |
Preparation Method | A low concentration of TGF-β (0.01ng/ml) was used for Treg culture. DMSO, Dehydrolithocholic acid (20μM) or isoalloLCA (20μM) was added on day 0 and CD4+ T cells were gated for analyses on day 3 for Th17 and Treg, day 5 for Th1 and Th2. |
Reaction Conditions | 20μM；48h |
Applications | Dehydrolithocholic acid can inhibit Th 17 differentiation of cells and reduce IL-17 α expression levels, but does not affect T cell differentiation into Th 1 or Th 2 cells |
| Animal experiment [1]: | |
Animal models | C57BL/6J mice from Jackson Laboratories (Jax) |
Preparation Method | Jax-B6 mice were fed with fecal slurry containing SFB (segmented filamentous bacteria from C57 BL/6 NTac mice) and fed with a control diet or a diet containing 0.3% (w/w) Dehydrolithocholic acid for one week. The average concentration of Dehydrolithocholic acid in the cecal contents is 24picomol/mg wet weight (approximately equivalent to μM) |
Dosage form | 0.3% (w/w) dietary administration |
Applications | Dehydrolithocholic Acid treatment significantly reduced the percentage of Th17 cells in the ileum |
References: | |
| Cas No. | 1553-56-6 | SDF | |
| Synonyms | 3-keto LCA, 3-keto Lithocholate, 3-keto Lithocholic Acid, 3-KLCA, 3-oxo LCA, 3-oxo Lithocholate, 3-oxo Lithocholic Acid | ||
| Canonical SMILES | C[C@H](CCC(O)=O)[C@@]1([H])CC[C@@]2([H])[C@]3([H])CC[C@]4([H])CC(CC[C@]4(C)[C@@]3([H])CC[C@@]21C)=O | ||
| Formula | C24H38O3 | M.Wt | 374.6 |
| Solubility | DMF: 30 mg/ml,DMF:PBS (pH 7.2) (1:4): 0.20 mg/ml,DMSO: 15 mg/ml,Ethanol: 10 mg/ml | Storage | Store at -20°C |
| General tips | Please select the appropriate solvent to prepare the stock solution according to the
solubility of the product in different solvents; once the solution is prepared, please store it in
separate packages to avoid product failure caused by repeated freezing and thawing.Storage method
and period of the stock solution: When stored at -80°C, please use it within 6 months; when stored
at -20°C, please use it within 1 month. To increase solubility, heat the tube to 37°C and then oscillate in an ultrasonic bath for some time. |
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| Shipping Condition | Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request. | ||
| Prepare stock solution | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.6695 mL | 13.3476 mL | 26.6951 mL |
| 5 mM | 0.5339 mL | 2.6695 mL | 5.339 mL |
| 10 mM | 0.267 mL | 1.3348 mL | 2.6695 mL |
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- Purity: >98.00%
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Average Rating: 5 (Based on Reviews and 35 reference(s) in Google Scholar.)
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