Deoxycholic acid sodium salt (Sodium deoxycholate) |
| カタログ番号GC33768 |
胆汁酸であるデオキシコール酸ナトリウム塩（デオキシコール酸ナトリウム）（デオキシコール酸ナトリウム）は、Gタンパク質共役胆汁酸受容体TGR5を活性化する腸代謝の副産物です。
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Cas No.: 302-95-4
Sample solution is provided at 25 µL, 10mM.
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Deoxycholic acid sodium salt (Sodium deoxycholate) is a bile acid that is a byproduct of intestinal metabolism and can activate the G protein-coupled bile acid receptor TGR5[1].
Deoxycholic acid sodium salt (Sodium deoxycholate) (100μM) induced the gastric cancer cell line MGC803 to produce cells resistant to acidified bile acids and enhanced its survival and proliferation activity under bile acid stress[1]. Deoxycholic acid sodium salt (Sodium deoxycholate) (50μM; 5min) inhibited PTPase activity in hepatocytes, thereby activating EGFR and MAPK pathways[2]. Deoxycholic acid sodium salt (Sodium deoxycholate) (50-150μM) significantly inhibited wound closure of cultured epithelial monolayer cells and attenuated cell migration in the Boyden chamber assay[3]. Deoxycholic acid sodium salt (Sodium deoxycholate) (0-300μM; 15h) reduced the gene expression of multiple pathways related to Caco-2 cell junctions (tight junctions, focal adhesions, gap junctions and adherens junction pathways) and increased permeability in a human intestinal barrier model [4]. Deoxycholic acid sodium salt (Sodium deoxycholate) (0-200μM; 24h) dose-dependently induced NLRP3 inflammasome activation and production of the highly proinflammatory cytokine IL-1β in macrophages [5].
Enema of Deoxycholic acid sodium salt (Sodium deoxycholate) (4mM in 1ml PBS; 7 days) resulted in a significant decrease in body weight and shortened colon length in mice, and a significant increase in fecal blood scores and MPO activity [5]. Deoxycholic acid sodium salt (Sodium deoxycholate) (20-300mg/kg; 10h) increased the nuclear damage induced by 1,2-dimethylhydrazine (DMH) in colonocytes in C57BL/6J mice [6].
References:
[1].Wang X, Sun L, Wang X, et al. Acidified bile acids enhance tumor progression and telomerase activity of gastric cancer in mice dependent on c‐Myc expression[J]. Cancer Medicine, 2017, 6(4): 788-797.
[2].Qiao L, Studer E, Leach K, et al. Deoxycholic acid (DCA) causes ligand-independent activation of epidermal growth factor receptor (EGFR) and FAS receptor in primary hepatocytes: inhibition of EGFR/mitogen-activated protein kinase-signaling module enhances DCA-induced apoptosis[J]. Molecular biology of the cell, 2001, 12(9): 2629-2645.
[3]. Mroz M S, Lajczak N K, Goggins B J, et al. The bile acids, deoxycholic acid and ursodeoxycholic acid, regulate colonic epithelial wound healing[J]. American Journal of Physiology-Gastrointestinal and Liver Physiology, 2018, 314(3): G378-G387.
[4]. Zeng H, Safratowich B D, Cheng W H, et al. Deoxycholic acid modulates cell-junction gene expression and increases intestinal barrier dysfunction[J]. Molecules, 2022, 27(3): 723.
[5]. Zhao S, Gong Z, Zhou J, et al. Deoxycholic acid triggers NLRP3 inflammasome activation and aggravates DSS-induced colitis in mice[J]. Frontiers in Immunology, 2016, 7: 536.
[6]. Suzuki K, Bruce W R. Increase by deoxycholic acid of the colonic nuclear damage induced by known carcinogens in C57BL/6J mice[J]. Journal of the National Cancer Institute, 1986, 76(6): 1129-1132.
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