Microbial Metabolite; isomer of Lithocholic acid

在 0.01% 的浓度下，异寡胆酸不会显着阻碍 CF5 和 M120 孢子的萌发和生长，但在 0.1% 的更高浓度下，则会显着阻碍 CF5 和 M120 孢子的萌发和生长。异石胆酸 (0.00003%) 显着降低菌株 CF5、BI9、M120 和 630 的毒素活性，并抑制 CD196、M68、CF5 和 BI9 的生长。除 R20291 和 M120 外，异石胆酸 (0.0003%) 会导致所有菌株的毒素活性显着下降[3]。

与常规饮食的大鼠相比，高脂肪饮食 (HFD) 组的粪便异石胆酸水平从第 28 天开始明显下降[4]。

研究了使用3α和3β氚化胆汁酸将鹅脱氧胆酸和石胆酸细菌转化为相应的3β-羟基差向异构体的机制。在与产气荚膜梭菌孵育20小时后，3-氧代胆汁酸转化为3-α-（85%）和3-β-（15%）羟基胆汁酸。当[3β-3H]鹅脱氧胆酸或[3β3-H]石胆酸与细菌一起孵育时，在水性介质中回收了大约75%的放射性，胆汁酸部分中大约15%的放射性与异胆汁酸的3α位置有关。当[3β-3H]鹅脱氧胆酸与未标记的3-氧代-5β胆酸一起孵育时，回收了氚化的石胆酸和异石胆酸。只有当假设存在3-氧代中间体，并且在3-氧代化合物的还原过程中，胆汁酸中的3-β氢被细菌辅酶（NAD+或NADP+）转移到异胆汁酸的3-α位时，才能解释这些结果[1]。

[1]. Transformation of bile acids into iso-bile acids by Clostridium perfringens: possible transport of 3 beta-hydrogen via the coenzyme. Hepatology. 1985;5(6):1126-1131.

[2]. The metabolism of lithocholic acid and lithocholic acid-3-alpha-sulfate by human fecal bacteria. Lipids. 1982;17(7):477-482.

[3]. Inhibition of spore germination, growth, and toxin activity of clinically relevant C. difficile strains by gut microbiota derived secondary bile acids. Anaerobe. 2017;45:86-100.

[4]. Alterations of Bile Acids and Gut Microbiota in Obesity Induced by High Fat Diet in Rat Model. J Agric Food Chem. 2019;67(13):3624-3632.

Isolithocholic acid is a monohydroxy-5beta-cholanic acid with a beta-hydroxy substituent at position 3. The 3beta-hydroxy epimer of lithocholic acid. It has a role as a human metabolite, a rat metabolite and a xenobiotic metabolite. It is a bile acid, a 3beta-hydroxy steroid, a monohydroxy-5beta-cholanic acid and a C24-steroid. It is a conjugate acid of an isolithocholate.
A bile acid formed from chenodeoxycholate by bacterial action, usually conjugated with glycine or taurine. It acts as a detergent to solubilize fats for absorption and is itself absorbed. It is used as cholagogue and choleretic.

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The changing epidemiology of Clostridium difficile infection over the past decades presents a significant challenge in the management of C. difficile associated diseases. The gastrointestinal tract microbiota provides colonization resistance against C. difficile, and growing evidence suggests that gut microbial derived secondary bile acids (SBAs) play a role. We hypothesized that the C. difficile life cycle; spore germination and outgrowth, growth, and toxin production, of strains that vary by age and ribotype will differ in their sensitivity to SBAs. C. difficile strains R20291 and CD196 (ribotype 027), M68 and CF5 (017), 630 (012), BI9 (001) and M120 (078) were used to define taurocholate (TCA) mediated spore germination and outgrowth, growth, and toxin activity in the absence and presence of gut microbial derived SBAs (deoxycholate, isodeoxycholate, lithocholate, isolithocholate, ursodeoxycholate, ω-muricholate, and hyodeoxycholate) found in the human and mouse large intestine. C. difficile strains varied in their rates of germination, growth kinetics, and toxin activity without the addition of SBAs. C. difficile M120, a highly divergent strain, had robust germination, growth, but significantly lower toxin activity compared to other strains. Many SBAs were able to inhibit TCA mediated spore germination and outgrowth, growth, and toxin activity in a dose dependent manner, but the level of inhibition and resistance varied across all strains and ribotypes. This study illustrates how clinically relevant C. difficile strains can have different responses when exposed to SBAs present in the gastrointestinal tract. [3]

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Obesity has become a worldwide health issue and has attracted much public attention. In the current study, we aim to elucidate the roles of bile acids and their associations with gut microbiota during obesity development, employing high fat diet (HFD)-induced obesity in a rat model. We collected feces and plasma, liver tissues, and segments of intestinal tissues and a developed bile acids quantification method by employing an ultraperformance liquid chromatography coupled with mass spectrometry detection (UPLC-MS) strategy. We then assessed bile acids fluxes in the biological matrixes collected. We found that, irrespective of dietary regimes, taurine-conjugated bile acids were the dominant species in the liver whereas unconjugated bile acids were in plasma. However, HFD caused slight increases in the total bile acids pool and particularly the increases in the levels of deoxycholic acid (DCA) (138.67 ± 37.225 nmol/L in control group, 242.61 ± 43.16 nmol/L in HFD group, p = 0.014) and taurodeoxycholic acid (TDCA) (2.8 ± 0.247 nmol/g in control group, 4.5 ± 0.386 nmol/g in HFD group, p = 0.0018) in plasma and liver tissues, respectively, which were consistent with the increased levels of DCA in intestinal tissues and feces. These changes are correlated to an increase in abundance of genera Blautia, Coprococcus, Intestinimonas, Lactococcus, Roseburia, and Ruminococcus. Our investigation revealed the fluxes of bile acids and their association with gut microbiota during obesity development and explicated unfavorable impact of HFD on health.[4]

C24H40O3

376.57

376.297

C, 76.55; H, 10.71; O, 12.75

1534-35-6

Lithocholic acid;434-13-9;Isoallolithocholic acid;2276-93-9

164853

White to off-white solid powder

1.1±0.1 g/cm3

511.0±23.0 °C at 760 mmHg

276.9±19.1 °C

0.0±3.0 mmHg at 25°C

1.528

6.7

57.5

2

3

4

27

574

9

C[C@H](CCC(=O)O)[C@H]1CC[C@@H]2[C@@]1(CC[C@H]3[C@H]2CC[C@H]4[C@@]3(CC[C@@H](C4)O)C)C

SMEROWZSTRWXGI-WFVDQZAMSA-N

InChI=1S/C24H40O3/c1-15(4-9-22(26)27)19-7-8-20-18-6-5-16-14-17(25)10-12-23(16,2)21(18)11-13-24(19,20)3/h15-21,25H,4-14H2,1-3H3,(H,26,27)/t15-,16-,17+,18+,19-,20+,21+,23+,24-/m1/s1

(4R)-4-[(3S,5R,8R,9S,10S,13R,14S,17R)-3-hydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoic acid

Isolithocholic acid; 1534-35-6; beta-Lithocholic acid; 3-Epilithocholic acid; beta-Lithocholanic acid; (4R)-4-[(3S,5R,8R,9S,10S,13R,14S,17R)-3-hydroxy-10,13-dimethyl-2,3,4,5,6,7,8,9,11,12,14,15,16,17-tetradecahydro-1H-cyclopenta[a]phenanthren-17-yl]pentanoic acid; 3beta-Hydroxy-5beta-cholan-24-oic Acid; Iso-LCA;

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO: 28.57 mg/mL (75.87 mM)

配方 1 中的溶解度: ≥ 2.86 mg/mL (7.59 mM) (饱和度未知) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将100 μL 28.6 mg/mL澄清DMSO储备液加入400 μL PEG300中，混匀；然后向上述溶液中加入50 μL Tween-80，混匀；加入450 μL生理盐水定容至1 mL。
*生理盐水的制备：将 0.9 g 氯化钠溶解在 100 mL ddH₂O中，得到澄清溶液。

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配方 2 中的溶解度: ≥ 2.86 mg/mL (7.59 mM) (饱和度未知) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 28.6 mg/mL 澄清 DMSO 储备液加入 900 μL 20% SBE-β-CD 生理盐水溶液中，混匀。
*20% SBE-β-CD 生理盐水溶液的制备（4°C，1 周）：将 2 g SBE-β-CD 溶解于 10 mL 生理盐水中，得到澄清溶液。

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配方 3 中的溶解度: ≥ 2.86 mg/mL (7.59 mM) (饱和度未知) in 10% DMSO + 90% Corn Oil (这些助溶剂从左到右依次添加，逐一添加), 澄清溶液。
例如，若需制备1 mL的工作液，可将 100 μL 28.6 mg/mL 澄清 DMSO 储备液加入900 μL 玉米油中，混合均匀。

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请根据您的实验动物和给药方式选择适当的溶解配方/方案：
1、请先配制澄清的储备液(如：用DMSO配置50 或 100 mg/mL母液(储备液));
2、取适量母液，按从左到右的顺序依次添加助溶剂，澄清后再加入下一助溶剂。以 下列配方为例说明 (注意此配方只用于说明，并不一定代表此产品 的实际溶解配方):
10% DMSO → 40% PEG300 → 5% Tween-80 → 45% ddH2O (或 saline);
假设最终工作液的体积为 1 mL, 浓度为5 mg/mL: 取 100 μL 50 mg/mL 的澄清 DMSO 储备液加到 400 μL PEG300 中，混合均匀/澄清；向上述体系中加入50 μL Tween-80，混合均匀/澄清；然后继续加入450 μL ddH2O (或 saline)定容至 1 mL；
3、溶剂前显示的百分比是指该溶剂在最终溶液/工作液中的体积所占比例;
4、 如产品在配制过程中出现沉淀/析出，可通过加热(≤50℃)或超声的方式助溶;
5、为保证最佳实验结果，工作液请现配现用！
6、如不确定怎么将母液配置成体内动物实验的工作液，请查看说明书或联系我们;
7、 以上所有助溶剂都可在 Invivochem.cn网站购买。