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.
Deoxycholic acid sodium salt (Sodium deoxycholate)是一种胆汁酸，是肠道代谢的副产物，可激活 G 蛋白偶联胆汁酸受体 TGR5[1]。
Deoxycholic acid sodium salt (Sodium deoxycholate)（100μM）诱导胃癌细胞系MGC803产生对酸化胆汁酸具有抗性的细胞，并增强其在胆汁酸应激下的存活和增殖活性[1]。Deoxycholic acid sodium salt (Sodium deoxycholate)（50μM；5min）抑制肝细胞中的PTPase活性，从而激活EGFR和MAPK通路[2]。Deoxycholic acid sodium salt (Sodium deoxycholate)（50-150μM）显著抑制培养上皮单层细胞的伤口闭合，并在Boyden室测定中减弱细胞迁移[3]。Deoxycholic acid sodium salt (Sodium deoxycholate)（0-300μM；15h）降低了与Caco-2细胞连接（紧密连接、粘着斑、缝隙连接和黏着连接通路）相关的多种通路的基因表达，并增加了人肠道屏障模型中的通透性[4]。Deoxycholic acid sodium salt (Sodium deoxycholate)（0-200μM；24h）剂量依赖性地诱导巨噬细胞中NLRP3炎症小体活化和高度促炎细胞因子IL-1β的产生[5]。
Deoxycholic acid sodium salt (Sodium deoxycholate)（4mM in 1ml PBS；7 days）灌肠导致小鼠体重显著下降和结肠长度缩短，粪便血液评分和MPO活性显著增加[5]。Deoxycholic acid sodium salt (Sodium deoxycholate)（20-300mg/kg；10h）增加了1,2-二甲基肼（1,2-dimethylhydrazine；DMH）在C57BL / 6J小鼠中引起的结肠细胞中核损伤[6]。