Indoxyl Sulfate (potassium salt)
(Synonyms: 硫酸吲哚钾盐) 目录号 : GC43903
Indoxyl Sulfate (IS), also known as 3-indoxylsulfate and 3-indoxylsulfuric acid, is a metabolite of dietary L-tryptophan that acts as a cardiotoxin and uremic toxin[1].
Cas No.:2642-37-7
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1]: | |
|
Cell lines |
Caco2 cells |
|
Preparation Method |
Cells treated with various concentrations of Indoxyl Sulfate for 24 hours. |
|
Reaction Conditions |
62.5-1000µM;24h |
|
Applications |
Indoxyl Sulfate (IS) induces intestinal damage via inhibiting mitophagic flux in Caco2 cells. |
| Animal experiment [2]: | |
|
Animal models |
C57BL/6J mice |
|
Preparation Method |
Mice were intraperitoneally injected with Indoxyl Sulfate (100 mg/kg) daily for 8 weeks. |
|
Dosage form |
100 mg/kg; i.p; 8 weeks |
|
Applications |
After injection of Indoxyl Sulfate, the intestinal macroscopical damage and permeability of mice increased, and the serum Indoxyl Sulfate level increased. |
|
References: [1]. Huang Y, Zhou J, et,al. Indoxyl sulfate induces intestinal barrier injury through IRF1-DRP1 axis-mediated mitophagy impairment. Theranostics. 2020 Jun 5;10(16):7384-7400. doi: 10.7150/thno.45455. PMID: 32641998; PMCID: PMC7330852. |
|
Indoxyl Sulfate (IS), also known as 3-indoxylsulfate and 3-indoxylsulfuric acid, is a metabolite of dietary L-tryptophan that acts as a cardiotoxin and uremic toxin[1]. Indoxyl Sulfate is taken up by proximal tubular cells through organic anion transporters (OAT1, OAT3), and it induces reactive oxygen species (ROS) with impairment of cellular antioxidative system[2-3].
Indoxyl Sulfate (62.5-1000µM;24h) induces intestinal damage via inhibiting mitophagic flux in Caco2 cells[4]. Indoxyl Sulfate (1 mM;12 h) induces fibrotic responses of tubular epithelial cells, renal fibroblasts, and macrophages via mTORC1 signaling [5]. Indoxyl Sulfate (1 mM;24 h) induces monocyte chemoattractant protein-1 (MCP-1) expression and reactive oxygen species (ROS) production in the differentiated 3T3L-1 adipocyte[6].
After injection of Indoxyl Sulfate (100 mg/kg; i.p; 8 weeks), the intestinal macroscopical damage and permeability of mice increased, and the serum Indoxyl Sulfate level increased [4]. Indoxyl Sulfate (10-3 M, 60 min) augments ET-1-induced contraction in rat aortae [7]. Indoxyl Sulfate (200 mg/kg/day of Indoxyl Sulfate in water) downregulates renal expression of Nrf2 through activation of NF-κB, followed by downregulation of HO-1 and NQO1 and increased production of ROS[8]. Indoxyl Sulfate increased endothelin-1-induced contraction but had no effect on phenylephrine, thromboxane analog, or isotonic K+-induced renal arterial contractions[9].
硫酸吲哚酚(Indoxyl sulfate (IS)),又称3-吲哚酚硫酸和3-吲哚酚硫酸,是膳食l -色氨酸的代谢物,具有心脏毒素和尿毒症毒素的作用[1]。Indoxyl Sulfate (IS)通过有机阴离子转运体(OAT1, OAT3)被近端小管细胞吸收,诱导活性氧(ROS),损害细胞抗氧化系统[2-3]。
Indoxyl Sulfate (62.5 ~ 1000µM;24h)通过抑制Caco2细胞的有丝分裂通量诱导肠道损伤[4]。Indoxyl Sulfate (1 mM;12 h)通过mTORC1信号传导诱导小管上皮细胞、肾成纤维细胞和巨噬细胞的纤维化反应[5]。Indoxyl Sulfate (1 mM;24 h)诱导分化的3T3L-1脂肪细胞单核细胞趋化蛋白-1 (MCP-1)表达和活性氧(ROS)产生[6]。
注射Indoxyl Sulfate后(100 mg/kg; i.p; 8 weeks), 小鼠肠道宏观损伤和通透性增加,血清Indoxyl Sulfate水平升高[4]。硫酸吲哚酚(10-3 M, 60 min)增强ET -1诱导的大鼠主动脉收缩[7]。硫酸吲哚酚(200 mg/kg/day of Indoxyl Sulfate in water)通过激活NF-κB下调肾脏Nrf2的表达,随后下调HO-1和NQO1,增加ROS的产生[8]。硫酸吲哚酚增加内皮素-1诱导的收缩,但对苯肾上腺素、血栓素类似物或等渗K+诱导的肾动脉收缩没有影响[9]。
References:
[1]. Lano G, Burtey S, et,al. Indoxyl Sulfate, a Uremic Endotheliotoxin. Toxins (Basel). 2020 Apr 5;12(4):229. doi: 10.3390/toxins12040229. PMID: 32260489; PMCID: PMC7232210.
[2]. Niwa T, Shimizu H. Indoxyl sulfate induces nephrovascular senescence. J Ren Nutr. 2012 Jan;22(1):102-6. doi: 10.1053/j.jrn.2011.10.032. PMID: 22200425.
[3]. Niwa T. Indoxyl sulfate is a nephro-vascular toxin. J Ren Nutr. 2010 Sep;20(5 Suppl):S2-6. doi: 10.1053/j.jrn.2010.05.002. PMID: 20797565.
[4]. Huang Y, Zhou J, et,al. Indoxyl sulfate induces intestinal barrier injury through IRF1-DRP1 axis-mediated mitophagy impairment. Theranostics. 2020 Jun 5;10(16):7384-7400. doi: 10.7150/thno.45455. PMID: 32641998; PMCID: PMC7330852.
[5]. Nakano T, Watanabe H, et,al.Indoxyl Sulfate Contributes to mTORC1-Induced Renal Fibrosis via The OAT/NADPH Oxidase/ROS Pathway. Toxins (Basel). 2021 Dec 18;13(12):909. doi: 10.3390/toxins13120909. PMID: 34941746; PMCID: PMC8706756.
[6]. Tanaka S, Watanabe H, et,al. Indoxyl Sulfate Contributes to Adipose Tissue Inflammation through the Activation of NADPH Oxidase. Toxins (Basel). 2020 Aug 5;12(8):502. doi: 10.3390/toxins12080502. PMID: 32764271; PMCID: PMC7472142.
[7]. Matsumoto T, Takayanagi K, et,al. Indoxyl sulfate enhances endothelin-1-induced contraction via impairment of NO/cGMP signaling in rat aorta. Pflugers Arch. 2021 Aug;473(8):1247-1259. doi: 10.1007/s00424-021-02581-8. Epub 2021 May 22. Erratum in: Pflugers Arch. 2021 Jun 17;: PMID: 34021781.
[8]. Bolati D, Shimizu H, et,al. Indoxyl sulfate, a uremic toxin, downregulates renal expression of Nrf2 through activation of NF-κB. BMC Nephrol. 2013 Mar 4;14:56. doi: 10.1186/1471-2369-14-56. PMID: 23496811; PMCID: PMC3599003.
[9]. Matsumoto T, Taguchi N, et,al. Indoxyl sulfate decreases uridine adenosine tetraphosphate-induced contraction in rat renal artery. Pflugers Arch. 2022 Dec;474(12):1285-1294. doi: 10.1007/s00424-022-02755-y. Epub 2022 Oct 1. PMID: 36181534.
| Cas No. | 2642-37-7 | SDF | |
| 别名 | 硫酸吲哚钾盐 | ||
| 化学名 | 3-(hydrogen sulfate), 1H-indol-3-ol, monopotassium salt | ||
| Canonical SMILES | [O-]S(OC1=CNC2=CC=CC=C21)(=O)=O.[K+] | ||
| 分子式 | C8H6NO4S • K | 分子量 | 251.3 |
| 溶解度 | 30mg/mL in DMSO or DMF | 储存条件 | Store at -20°C, protect from light |
| 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。 |
||
| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 3.9793 mL | 19.8965 mL | 39.7931 mL |
| 5 mM | 0.7959 mL | 3.9793 mL | 7.9586 mL |
| 10 mM | 0.3979 mL | 1.9897 mL | 3.9793 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
A robust, accurate, sensitive LC-MS/MS method to measure Indoxyl Sulfate, validated for plasma and kidney cells
Biomed Chromatogr 2022 May;36(5):e5307.PMID:34978088DOI:10.1002/bmc.5307.
Proximal tubular damage is an important prognostic determinant in various chronic kidney diseases (CKDs). Currently available diagnostic methods do not allow for early disease detection and are neither efficient. Indoxyl Sulfate (IS) is an endogenous metabolite and protein-bound uremic toxin that is eliminated via renal secretion, but accumulates in plasma during tubular dysfunction. Therefore, it may be suitable as a tubular function marker. To evaluate this, a fast bioanalytical method was developed and validated for IS in various species and a kidney cell line using LC-MS/MS. An isotope-labeled IS potassium salt as an internal standard and acetonitrile (ACN) as a protein precipitant were used for sample pretreatment. The analyte was separated on a Polaris 3 C18-A column by gradient elution using 0.1% formic acid in water and ACN, and detected by negative electrospray ionization in selected reaction monitoring mode. The within-day (≤ 4.0%) and between-day (≤ 4.3%) precisions and accuracies (97.7 to 107.3%) were within the acceptable range. The analyte showed sufficient stability at all conditions investigated. Finally, applying this assay, significantly higher plasma and lower urine concentrations of IS were observed in mice with diabetic nephropathy with tubular damage, which encourages validation toward its use as a biomarker.
Safety and efficacy of using cereal food (Frugra®) to improve blood pressure and bowel health in patients undergoing chronic hemodialysis: A pilot study
J Pharmacol Sci 2021 Sep;147(1):132-137.PMID:34294364DOI:10.1016/j.jphs.2021.06.007.
Hypertension and constipation are major hemodialysis complications. Salt restriction is one of the most important nonpharmacological interventions in managing hypertension. In patients undergoing hemodialysis, nonpharmacological strategies to manage constipation are extremely difficult to develop owing to the presence of excess dietary potassium and fluids. Frugra®, which is a cereal food that has a low salt content of 0.5 g per serving, may help reduce salt intake. Additionally, Frugra is rich in dietary fiber, thereby beneficial for such patients. In this study, we evaluated the safety and efficacy of Frugra in patients undergoing hemodialysis, focusing mainly on blood pressure and bowel health by changing the usual breakfast meal to Frugra for 8 weeks. We enrolled 11 patients undergoing hemodialysis. Despite the absence of changes in the patients' dry weight levels, their systolic blood pressure levels decreased from 155.5 ± 20.9 mmHg to 137.9 ± 10.3 mmHg after 2 months (P < 0.05). All participants reported improvements in bowel movement, and the levels of Indoxyl Sulfate, a representative gut-derived uremic toxin, were decreased from 49.3 μg/ml to 33.4 μg/ml. Furthermore, adverse events including electrolyte abnormalities were not observed. Therefore, Frugra may be useful to manage the health of patients undergoing hemodialysis.
[Pernicious anemia with indicanuria]
Rinsho Ketsueki 1989 Apr;30(4):578-82.PMID:2504979doi
A 67-year-old female was diagnosed as having classical pernicious anemia. Laboratory data included low serum vitamin B12 concentrations, abnormal deoxyuridine suppression test, methylmalonic aciduria, atrophic gastritis, positive anti-intrinsic factor antibody and Schilling test results typical of pernicious anemia. During hospitalization it was incidentally noted that her urine was green colored. Jaffe' reaction and Obermayer reaction for indicanuria were both positive. Dark purple crystalline material was obtained by centrifugation of her urine. The crystalline substance was soluble in methanol and its absorbance curve was identical to that of authentic indoxylsulphate potassium salt. Daily output of this substance was nearly 50 times normal. There was no increase in urinary excretion of monoamino-monocarboxyl amino acides. The exact reason for her indicanuria was not clear, although abnormal bacterial growth in the intestine remained as a possibility.