Glabridin, a functional compound of liquorice, attenuates colonic inflammation in mice with dextran sulphate sodium-induced colitis

Abstract

SummaryInflammatory bowel disease (IBD) is characterized by detrimental immune reactivity in the gut, and the imbalance between proinflammatory and antiinflammatory reactivity. The aims of this study were to determine whether oral administration of glabridin, a functional component of liquorice, could ameliorate dextran sulphate sodium (DSS)-induced colitis, as well as to understand the possible underlying mechanisms. Acute experimental colitis was induced in BALB/c mice by treatment with 5% DSS for 7 days. Glabridin (10 or 50 mg/kg/day) was given for 7 days. Treatment with glabridin significantly attenuated mortality, loss of body weight, shortening of the colon and severe clinical symptoms. This was associated with a remarkable amelioration of the disruption of the colonic architecture, a significant reduction in colonic myeloperoxidase (MPO) activity and the production of inflammatory mediators such as nitric oxide (NO), prostaglandin (PG) E2, and proinflammatory cytokines. These results suggest that glabridin-mediated anti-inflammatory action on colorectal sites may be a useful therapeutic approach to IBD.

Glabridin inhibits lipopolysaccharide‐induced activation of a microglial cell line, BV‐2, by blocking NF‐κB and AP‐1

“…The results demonstrated that the mRNA expression of these infl ammatory mediators are dose-dependently suppressed by glabridin treatment, suggesting that the inhibitory effect of glabridin on the production of NO, TNF-α and IL-1β might be mediated by the inhibition of mRNA expression of cognate genes. Consistent with our results, Kwon and coworkers recently reported that glabridin attenuates colonic infl ammation by inhibiting the expression of infl ammatory mediators, such as NO, PGE 2 and TNF-α (Kwon et al, 2008). It was also reported previously that glabridin inhibits NO production and iNOS gene expression in mouse peritoneal macrophages and RAW 264.7 cells, a mouse macrophage cell line (Kang et al, 2005).…”

AMPK activation with glabridin ameliorates adiposity and lipid dysregulation in obesity

“…In differentiated adipocytes, glabridin stimulated AMPK phosphorylation and decreased expression of proinfl ammatory genes in the presence of TNF ␣ , a potent infl ammatory inducer. Consistent with these data, glabridin exhibits anti-infl ammatory responses in colitic subjects ( 60 ). Therefore, it appears that glabridin-induced AMPK might also contribute to the suppression of infl ammatory responses, which would lead to improvements in metabolic disorders, such as insulin resistance in obesity.…”

Glabridin Inhibits Migration, Invasion, and Angiogenesis of Human Non–Small Cell Lung Cancer A549 Cells by Inhibiting the FAK/Rho Signaling Pathway

“…7 The root of Glycyrrhiza glabra (licorice) has been used for many centuries in Asia and Europe as an antioxidant, antidote, demulcent, expectorant, and a remedy for allergic inflammation, as well as a flavoring and sweetening agent. 8 Glabridin, an active isoflavan in the hydrophobic fraction of licorice root, 9,10 is easily incorporated into the gut cells and released to the basolateral side by aglycone form in human 1 and mice. 11,12 It has shown multiple biological activities, such as antibacterial, neuroprotective, antiatherosclerotic, antiosteoporosis, and immunomodulatory activities.…”

“…11,12 It has shown multiple biological activities, such as antibacterial, neuroprotective, antiatherosclerotic, antiosteoporosis, and immunomodulatory activities. [9][10][11][12][13][14][15][16][17] Studies have shown that glabridin exhibits growth inhibition properties against breast cancer cells. 17 It also enhances the efficacy of cancer chemotherapy by inhibiting P-glycoprotein and multidrug resistance protein 1 synthesis.…”