Hippuric acid (2-Benzamidoacetic acid)
(Synonyms: 马尿酸,2-Benzamidoacetic acid) 目录号 : GC33778
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Hippuric acid (2-Benzamidoacetic acid) 是一种口服活性代谢物。
Cas No.:495-69-2
Sample solution is provided at 25 µL, 10mM.
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Hippuric acid (2-Benzamidoacetic acid) is an orally active metabolite[1]. Hippuric acid can be produced by the metabolism of polyphenols and benzoic acid by gut microbiota[2]. Hippuric acid is usually used in the study of cardiovascular diseases, metabolic diseases, and inflammation/immunology[3][4].
In vitro, treatment of RAW 264.7 cells and primary mouse bone marrow cells with Hippuric acid (60µg/dL; 4-5days) significantly inhibited osteoclastogenesis and osteoclast resorptive activity[5].
In vivo, Hippuric acid (100mg/kg; intraperitoneal injection; five times per week for 10 weeks) significantly increased serum creatinine and blood urea nitrogen levels, promoted renal fibrosis, and disrupted redox homeostasis in a 5/6 nephrectomy rat model of chronic kidney disease[6]. Hippuric acid (150mg/kg/day; p.o.; 7 days) significantly reduced disease activity index (DAI) scores, colon shortening, and histological inflammation scores, increased colon length, and alleviated histopathological damage in the colon of DSS-induced colitis mice[7].
References:
[1] Nativelle C, Picard K, Valentin I, Lhuguenot JC, Chagnon MC. Metabolism of n-butyl benzyl phthalate in the female Wistar rat. Identification of new metabolites. Food Chem Toxicol. 1999;37(8):905-917.
[2] Edwards SJ, Carter S, Nicholson T, et al. (-)-Epicatechin and its colonic metabolite hippuric acid protect against dexamethasone-induced atrophy in skeletal muscle cells. J Nutr Biochem. 2022;110:109150.
[3] Pero RW. Health consequences of catabolic synthesis of hippuric acid in humans. Curr Clin Pharmacol. 2010;5(1):67-73.
[4] Santhakumar AB, Stanley R, Singh I. The ex vivo antiplatelet activation potential of fruit phenolic metabolite hippuric acid. Food Funct. 2015;6(8):2679-2683.
[5] Zhao H, Lazarenko OP, Chen JR. Hippuric acid and 3-(3-hydroxyphenyl) propionic acid inhibit murine osteoclastogenesis through RANKL-RANK independent pathway. J Cell Physiol. 2020;235(1):599-610.
[6] Sun B, Wang X, Liu X, et al. Hippuric Acid Promotes Renal Fibrosis by Disrupting Redox Homeostasis via Facilitation of NRF2-KEAP1-CUL3 Interactions in Chronic Kidney Disease. Antioxidants (Basel). 2020;9(9):783.
[7] Yang Y, Huang S, Liao Y, et al. Hippuric acid alleviates dextran sulfate sodium-induced colitis via suppressing inflammatory activity and modulating gut microbiota. Biochem Biophys Res Commun. 2024;710:149879.
Hippuric acid (2-Benzamidoacetic acid) 是一种口服活性代谢物[1]。Hippuric acid可由肠道微生物代谢多酚和苯甲酸产生[2]。Hippuric acid通常用于心血管疾病、代谢性疾病和炎症/免疫学的研究[3][4]。
体外实验中，用Hippuric acid（60µg/dL；4-5天）处理RAW 264.7细胞和原代小鼠骨髓细胞，显著抑制了破骨细胞生成和破骨细胞的吸收活性[5]。
体内实验中，Hippuric acid（100mg/kg；腹腔注射；每周5次，持续10周）显著增加了5/6肾切除慢性肾脏病（CKD）大鼠血清肌酐和血尿素氮水平，促进了肾纤维化，并破坏了氧化还原平衡[6]。Hippuric acid（150mg/kg/天；口服；7天）显著降低了DSS诱导的结肠炎小鼠的疾病活动指数（DAI）评分、结肠缩短和组织学炎症评分，增加了结肠长度，并减轻了结肠的组织病理学损伤[7]。
| Cell experiment [1]: | |
Cell lines | RAW 264.7 cells and primary mouse bone marrow cells |
Preparation Method | Non adherent bone marrow cells from 4‐week‐old female C57BL/J mice were isolated. Bone marrow cells were flushed from femurs and then cultured in T175 Flasks for 2 days to let stromal cells attach. Two days later, non adherent cells were collected and cultured in appropriate plates with appropriate cell densities. These cells are considered as hematopoietic osteoclast progenitor cells. Conditional serum for treatment of cells was taken from female rats either fed 10% BB supplemental diet or standard rodent casein diet for 4 weeks. RAW 264.7 cells and primary mouse bone marrow cells were cultured in α‐Minimum Essential Medium supplemented with 10% fetal bovine serum, penicillin (100units/ml), streptomycin (100µg/ml), and glutamine (4mM). Cells were seeded in 96‐, 12‐, or 6‐well cell culture plates at appropriate density of cells per well for morphology, RNA, and protein expression experiments. At 85% confluence, cells in 96‐well plates were treated with 2.5% rat serum (7.5% FBS) in the presence of 50ng/ml of soluble RANKL for osteoclastic cell morphologic study. RAW264.7 cells or nonadherent bone marrow cells were cultured in 96‐well plates (2×104 cells/well) in the presence or absence of 50ng/ml of RANKL. Cells were treated with 60µg/dL Hippuric acid. After 4 days for RAW264.7 cell cultures and 5 days for bone marrow cell cultures, the cells were fixed with 4% paraformaldehyde and stained for tartrate‐resistant acid phosphatase (TRAPase) activity using a TRAPase Staining Kit. TRAP‐positive cells containing >3 nuclei in each well were counted as osteoclasts under an epifluorescent microscope. For osteoclast resorption activity assay, cells in the culture plates were fixed using 2.5% glutaraldehyde with or without Von Kossa staining. The areas of hydroxyapatite resorption were observed by light microscopy and analyzed using the Image J software. Cell viability was measured by MTT assay. |
Reaction Conditions | 60µg/dL; 4-5days |
Applications | Treatment of RAW 264.7 cells and primary mouse bone marrow cells with Hippuric acid significantly inhibited osteoclastogenesis and osteoclast resorptive activity. |
| Animal experiment [2]: | |
Animal models | Male Sprague Dawley rats |
Preparation Method | Male Sprague Dawley rats at the age of 7 weeks were housed in a pathogen-free environment. The environment was that with a humidity of 50-70%, temperature of 22-24℃, and the day and night cycle was 12/12h. These rats were given a normal laboratory diet with ad libitum access to water. After 1 week of adaptation, fifty rats were subjected to either sham surgery (kidney exposure operation only) or 5/6NX surgery. The 5/6NX model commonly used to simulate typical CKD symptoms and study PUBT-promoted renal fibrosis. Two weeks after surgery (experimental week 1), excluding the rats that died during the operation, rats in the sham group (n=9) were treated with vehicle (0.5% DMSO), and 5/6NX rats were randomized into two groups (n=9 each) and treated as follows: (1) a 5/6NX group, 0.5% DMSO; (2) a 5/6NX + Hippuric acid group, 100mg/kg Hippuric acid. All treatments were administered intraperitoneally, five times per week for 10 weeks. Rats serum creatinine (SCr) and blood urea nitrogen (BUN) contents were evaluated using a BS-420 automated biochemical analyzer. Kidney samples were fixed for histological and immunohistochemical analyses. Total intracellular ROS and H2O2 concentrations were determined using commercial ROS and H2O2 assay kits. |
Dosage form | 100mg/kg; intraperitoneal injection; five times per week for 10 weeks |
Applications | Hippuric acid significantly increased serum creatinine and blood urea nitrogen levels, promoted renal fibrosis, and disrupted redox homeostasis in a 5/6 nephrectomy rat model of chronic kidney disease. |
References: | |
| Cas No. | 495-69-2 | SDF | |
| 别名 | 马尿酸,2-Benzamidoacetic acid | ||
| Canonical SMILES | O=C(O)CNC(C1=CC=CC=C1)=O | ||
| 分子式 | C9H9NO3 | 分子量 | 179.17 |
| 溶解度 | DMSO : ≥ 100 mg/mL (558.13 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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| 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 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 5.5813 mL | 27.9065 mL | 55.8129 mL |
| 5 mM | 1.1163 mL | 5.5813 mL | 11.1626 mL |
| 10 mM | 558.1 μL | 2.7906 mL | 5.5813 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 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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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，
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2.
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- Purity: >99.00% Appearance: A solid
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