Monoammoniumglycyrrhizinate

Animal experiment:

Mice[1]In this study, BALB/c mice (male, 6-8weeks old, and 20-25 g) are used. Mice are randomly divided into five groups: control group, LPS group, and LPS + Monoammonium glycyrrhizinate (MAG: 3, 10, and 30mg/kg) groups. Each group contains eight mice. Mice are anesthetized with intraperitoneal injection of sodium pentobarbital (50mg/kg). Before inducing acute lung injury, the mice are given intraperitoneal injection with MAG (3, 10, and 30mg/kg). One hour later, LPS (5mg/kg) is instilled intratracheally to induce acute lung injury. Normal mice are given PBS[1]. Rats[2]Male Wistar rats (180-220 g) are used. Rats are randomly divided into four groups, i.e., control group, RIF and INH group, MAG low-dose group, and MAG high-dose group, each group has 15 rats. Rats in the RIF and INH group receive RIF (60 mg/kg) and INH (60 mg/kg) by gavage administration once daily; rats in MAG groups are pretreated with MAG at the doses of 45 or 90 mg/kg, RIF (60 mg/kg) and INH (60 mg/kg) are given 3 h after MAG administration; rats in the control group are treated with saline. To evaluate the dynamic effect of drugs, rats in each group are sacrificed on 7, 14, and 21 d after drug administration[2].

References:

[1]. Huang X, et al. Anti-Inflammatory Effects of Monoammonium Glycyrrhizinate on Lipopolysaccharide-Induced Acute Lung Injury in Mice through Regulating Nuclear Factor-Kappa B Signaling Pathway. Evid Based Complement Alternat Med. 2015;2015:272474.
[2]. Zhou L, et al. Monoammonium glycyrrhizinate protects rifampicin- and isoniazid-induced hepatotoxicity via regulating the expression of transporter Mrp2, Ntcp, and Oatp1a4 in liver. Pharm Biol. 2016;54(6):931-7.