18α-Glycyrrhetinic acid is a bioactive triterpenoid mainly derived from Glycyrrhiza radix. 18α-Glycyrrhetinic acid has various pharmacological activities such as anti-oxidative and anti-inflammatory[1]. 18α-Glycyrrhetinic acid can inhibit oxidative stress via activating Nrf-2 signaling[1].
18α-Glycyrrhetinic acid (8μM; 72h) inhibited cell growth in Human HSC cells[2]. 18α-Glycyrrhetinic acid (4μg/mL; 24h) significantly reduced ROS (reactive oxygen species) production in fructose-treated HK2 cells[3]. 18α-Glycyrrhetinic acid (50μM; 48h) decreased the cell viability in Caco-2 cells[4]. 18α-Glycyrrhetinic acid (2μg/mL; 24h) increased the cell viability in mitomycin C-induced HFL-1 cells[1].
18α-Glycyrrhetinic acid (10mg/kg; 30d; q2d; i.p.) significantly decreased the expression of CD40 and MHC-II molecules in BALB/c mice[5]. 18α-Glycyrrhetinic acid (12.5, 25 and 50mg/kg; 12 weeks; p.o.) alleviated fructose-induced renal injury in C57BL/6 mice[3].
References:[1] Lefaki M, Papaevgeniou N, Tur J A, et al. The dietary triterpenoid 18α-glycyrrhetinic acid protects from MMC-induced genotoxicity through the ERK/Nrf2 pathway [J]. Redox biology, 2020, 28: 101317.
[2] Zong L, Qu Y, Xu M Y, et al. 18α-Glycyrrhetinic acid extracted from Glycyrrhiza radix inhibits proliferation and promotes apoptosis of the hepatic stellate cell line [J]. Journal of digestive diseases, 2013, 14(6): 328-336.
[3] Cheng X, Qiu L, Wang F. 18α-Glycyrrhetinic acid (GA) ameliorates fructose-induced nephropathy in mice by suppressing oxidative stress, dyslipidemia and inflammation [J]. Biomedicine & pharmacotherapy, 2020, 125: 109702.
[4] Malekinejad M, Pashaee M R, Malekinejad H. 18β-Glycyrrhetinic acid altered the intestinal permeability in the human Caco-2 monolayer cell model [J]. European journal of nutrition, 2022, 61(7): 3437-3447.
[5] Ebrahimnezhad S, Amirghofran Z, Karimi M H. Decline in immunological responses mediated by dendritic cells in mice treated with 18α-glycyrrhetinic acid [J]. Immunological investigations, 2016, 45(3): 191-204.