Glycyrrhizic acid is a triterpenoid saponinl, acting as a direct HMGB1 antagonist, with anti-tumor, anti-diabetic activities.
体外研究 (In Vitro)
Glycyrrhizic acid shows a series of anti-cancer-related pharmacological activities, such as broad-spectrum anti-cancer ability, resistance to the tissue toxicity caused by chemotherapy and radiation, drug absorption enhancing effects and anti-multidrug resistance (MDR) mechanisms, as a carrier material in drug delivery systems[1]. In intestinal NCI-H716 cells that secretes GLP-1, Glycyrrhizic acid promotes GLP-1 secretion with a marked elevation of calcium levels. Glycyrrhizic acid can enhance GLP-1 secretion through TGR5 activation[2]. Glycyrrhizic acid can form a stable transparent low-molecular-weight hydrogels (LMWHs) at 37°C in physiological phosphate buffered saline (PBS) with nanoclusters as the microstructures[4].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
体内研究 (In Vivo)
In type 1-like diabetic rats induced by streptozotocin (STZ-treated rats), Glycyrrhizic acid increases the level of plasma GLP-1, which is blocked by triamterene at a dose sufficient to inhibit Takeda G-protein-coupled receptor 5 (TGR5)[1]. Glycyrrhizic acid (Glycyrrhizic acid; 50 mg/kg, i.p.) significantly decreases the levels of TgAb, HMGB1, TNF-α, IL-6, IL-1β in mice[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
分子量
822.93
Formula
C42H62O16
CAS 号
1405-86-3
中文名称
甘草酸;甘草皂甙;甘草甜素;强力宁;甘草皂苷
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Powder
-20deg;C
3 years
4deg;C
2 years
In solvent
-80deg;C
6 months
-20deg;C
1 month
溶解性数据
In Vitro:;
DMSO : 900 mg/mL (1093.65 mM; Need ultrasonic and warming)
[1]. Su X, et al. Glycyrrhizic acid: A promising carrier material for anticancer therapy. Biomed Pharmacother. 2017 Sep 5;95:670-678
[2]. Wang LY, et al. Glycyrrhizic acid increases glucagon like peptide-1 secretion via TGR5 activation in type 1-like diabetic rats. Biomed Pharmacother. 2017 Sep 4;95:599-604.
[3]. Li C, et al. Glycyrrhizin, a Direct HMGB1 Antagonist, Ameliorates Inflammatory Infiltration in a Model of Autoimmune Thyroiditis via Inhibition of TLR2-HMGB1 Signaling. Thyroid. 2017 May;27(5):722-731.
[4]. Xia Zhao, et al. A Simple Injectable Moldable Hydrogel Assembled from Natural Glycyrrhizic Acid with Inherent Antibacterial Activity. ACS Appl. Bio Mater. 2020, 3, 1, 648–653.
Animal Administration [3]
Mice[3] NOD.H-2h4 mice are fed in the animal house until 4 weeks of age. A total of 24 male mice are then randomly separated into three different groups (n=8 per group). Mice in the control group are given sterile water without supplement. Mice in the iodine supplement (NaI) group are given 0.005% NaI in the drinking water. Mice in the NaI+Glycyrrhizic acid group are treated with 50 mg/kg Glycyrrhizic acid once daily for 4 weeks, administered via intraperitoneal injection after 8 weeks of iodine supplementation. Thyroid tissues are removed surgically under anesthesia, washed with cold saline, blotted on filter paper and weighed using an electronic balance. The thyroid gland tissues are then stored at -80°C until use[3].
MCE has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Su X, et al. Glycyrrhizic acid: A promising carrier material for anticancer therapy. Biomed Pharmacother. 2017 Sep 5;95:670-678
[2]. Wang LY, et al. Glycyrrhizic acid increases glucagon like peptide-1 secretion via TGR5 activation in type 1-like diabetic rats. Biomed Pharmacother. 2017 Sep 4;95:599-604.
[3]. Li C, et al. Glycyrrhizin, a Direct HMGB1 Antagonist, Ameliorates Inflammatory Infiltration in a Model of Autoimmune Thyroiditis via Inhibition of TLR2-HMGB1 Signaling. Thyroid. 2017 May;27(5):722-731.
[4]. Xia Zhao, et al. A Simple Injectable Moldable Hydrogel Assembled from Natural Glycyrrhizic Acid with Inherent Antibacterial Activity. ACS Appl. Bio Mater. 2020, 3, 1, 648–653.
[1]. Lee SH, et al. Ameliorating effect of dipotassium glycyrrhizinate on an IL-4- and IL-13-induced atopic dermatitis-like skin-equivalent model. Arch Dermatol Res. 2019 Mar;311(2):131-140.