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]。
















