Glycodeoxycholic Acid
(Synonyms: 甘氨脱氧胆酸；甘氨去氧胆酸) 目录号 : GC38644
Glycodeoxycholic Acid是脱氧胆酸的甘氨酸结合形式。
Cas No.:360-65-6
Sample solution is provided at 25 µL, 10mM.
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Glycodeoxycholic Acid is a glycine-conjugated form of the secondary bile acid deoxycholic acid[1]. Glycodeoxycholic Acid participates in bile formation and fat digestion and absorption, and also plays an important role in regulating cholesterol metabolism and maintaining gut microbiota balance[2]. Glycodeoxycholic Acid is mainly used in the research of bile acid metabolism and related diseases[3].
In vitro, treatment of primary hepatocytes isolated from rats with Glycodeoxycholic Acid (250μM; 4h) significantly increased hepatocyte MDA levels, decreased membrane fluidity, elevated ALT levels, and induced hepatocyte injury[4]. Glycodeoxycholic Acid (0.5mM; 24h) significantly inhibited the proliferation and migration, and increased cells apoptosis in human hepatocellular carcinoma (HCC) SUN-449 and HepG2 cells[5].
In vivo, Glycodeoxycholic Acid (100mg/kg/day; oral gavage from postnatal day 11 to 34) delayed the onset of puberty, increased hypothalamic Sirt1 expression, and decreased serum LH levels, Kiss1 and GnRH expression in high-fat diet-induced central precocious puberty (CPP) female rats[6]. Intraduodenal infusion of Glycodeoxycholic Acid at a rate equivalent to the hepatic bile acid flux (32.90±9.04mg/h) for 24 hours reduced cholesterol 7α-hydroxylase activity and inhibited endogenous bile acid synthesis in the rabbit model with bile fistula[7].
References:
[1] Lefebvre P, Cariou B, Lien F, Kuipers F, Staels B. Role of bile acids and bile acid receptors in metabolic regulation. Physiol Rev. 2009;89(1):147-191.
[2] Jia Y, Yang X, Wilson LM, et al. Diet-Related and Gut-Derived Metabolites and Health Outcomes: A Scoping Review. Metabolites. 2022;12(12):1261.
[3] Farooqui N, Elhence A, Shalimar. A Current Understanding of Bile Acids in Chronic Liver Disease. J Clin Exp Hepatol. 2022;12(1):155-173.
[4] Huang W, Kang G, Tu Z. Zhonghua Gan Zang Bing Za Zhi. 1999;7(1):46-47.
[5] Shen R, Ke L, Li Q, et al. Abnormal bile acid-microbiota crosstalk promotes the development of hepatocellular carcinoma. Hepatol Int. 2022;16(2):396-411.
[6] Wu N, Jiang X, Liu Y, et al. Glycodeoxycholic acid alleviates central precocious puberty by modulating gut microbiota and metabolites in high-fat diet-fed female rats. Cell Mol Life Sci. 2025;82(1):163.
[7] Xu G, Salen G, Batta AK, et al. Glycocholic acid and glycodeoxycholic acid but not glycoursocholic acid inhibit bile acid synthesis in the rabbit. Gastroenterology. 1992;102(5):1717-1723.
Glycodeoxycholic Acid是脱氧胆酸的甘氨酸结合形式[1]。Glycodeoxycholic Acid参与胆汁的形成以及脂肪的消化吸收，并在调节胆固醇代谢和维持肠道微生物群平衡方面发挥重要作用[2]。Glycodeoxycholic Acid主要用于胆汁酸代谢及相关疾病的研究[3]。
在体外，用Glycodeoxycholic Acid（250μM；4小时）处理从大鼠分离的原代肝细胞，显著增加了肝细胞丙二醛（MDA）水平，降低了细胞膜流动性，提高了丙氨酸转氨酶（ALT）水平，并诱导肝细胞损伤[4]。Glycodeoxycholic Acid（0.5mM；24小时）显著抑制了人肝细胞癌（HCC）SUN-449和HepG2细胞的增殖和迁移，并增加了细胞凋亡[5]。
在体内，Glycodeoxycholic Acid（100mg/kg/天；从出生后第11天至第34天口服灌胃）延迟了高脂饮食诱导的中枢性性早熟（CPP）雌性大鼠的青春期发育，增加了下丘脑Sirt1表达，并降低了血清黄体生成素（LH）水平、Kiss1和GnRH表达[6]。在带有胆汁瘘的兔子模型中，以相当于肝脏胆汁酸通量（32.90±9.04mg/h）的速率进行24小时的Glycodeoxycholic Acid十二指肠内灌注降低了胆固醇7α-羟化酶活性，抑制了内源性胆汁酸合成[7]。
| Cell experiment [1]: | |
Cell lines | SUN-449 and HepG2 human HCC cell lines |
Preparation Method | SUN-449 and HepG2 human HCC cell lines were maintained in Dulbecco’s modified Eagle’s medium (DMEM) with 10% fetal bovine serum (FBS). Cells were cultured in a cell incubator with 5% CO2 at 37°C. And cells were treated with Glycodeoxycholic Acid (0.5mM) or PBS for 24h. Then CCK-8 and Transwell assays were performed for cell proliferation and migration detection. And cell apoptosis was detected using an Annexin V FITC apoptosis detection kit. |
Reaction Conditions | 0.5mM; 24h |
Applications | Glycodeoxycholic Acid significantly inhibited the proliferation and migration, and increased cells apoptosis in human hepatocellular carcinoma (HCC) SUN-449 and HepG2 cells. |
| Animal experiment [2]: | |
Animal models | Wistar rats |
Preparation Method | 6-8 weeks old male (330-360g) and female (215-250g) Wistar rats were housed in 22°C under constant lighting conditions (14/10h light/dark cycle) with ad libitum access to food and water. After a two-week adaptation period, two females were paired with one adult male Wistar rat to produce experimental female offspring. Subsequently, the rats were randomly divided into two groups: HFD (n=14) and NN (n=14). To model CPP, female pups were raised in small litters of four pups per dam starting on postnatal day (PND) 10 and given free access to HFD from PND 21 to PND 33. In contrast, the NN group consisted of female pups raised in normal litters of twelve pups per dam, fed a standard diet. Wistar rats in the CPP model were administered 100mg/kg/d Glycodeoxycholic Acid (diluted in sterile saline) via gavage from PND 11 to PND 34, while the control group received the same volume of the vehicle. Rat weights were recorded every four days from PND 10 to PND 21 and daily thereafter until the experiment ended. At the termination of the experiment, the rats were euthanized following a 16-hour fasting period. Blood samples were collected and centrifuged at 3500rpm for 15min at 4°C to obtain serum. The hypothalamus, uterus, ovaries, and feces were immediately collected, frozen in liquid nitrogen, and stored at -80°C until further analysis. In addition, the wet weights of the uterus and ovaries were measured, and the relative uterus weight (UW) and ovary weight (OW) (mg/100g) were calculated. Ovarian tissues were stained with hematoxylin and eosin after fixation in formalin. |
Dosage form | 100mg/kg/day; oral gavage from postnatal day 11 to 34 |
Applications | Glycodeoxycholic Acid delayed the onset of puberty, increased hypothalamic Sirt1 expression, and decreased serum LH levels, Kiss1 and GnRH expression in high-fat diet-induced central precocious puberty (CPP) female rats. |
References: | |
| Cas No. | 360-65-6 | SDF | |
| 别名 | 甘氨脱氧胆酸；甘氨去氧胆酸 | ||
| Canonical SMILES | C[C@@H]([C@]1(CC[C@]2([C@@]3(CC[C@@]4(C[C@@H](CC[C@@]4([C@]3(C[C@@H]([C@@]21C)O)[H])C)O)[H])[H])[H])[H])CCC(NCC(O)=O)=O | ||
| 分子式 | C26H43NO5 | 分子量 | 449.62 |
| 溶解度 | DMSO: 250 mg/mL (556.03 mM) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.2241 mL | 11.1205 mL | 22.241 mL |
| 5 mM | 444.8 μL | 2.2241 mL | 4.4482 mL |
| 10 mM | 222.4 μL | 1.1121 mL | 2.2241 mL |
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动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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2.
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