Glycyrrhizin enhances interleukin-10 production by liver dendritic cells in mice with hepatitis.
BACKGROUND
Glycyrrhizin (GL), an aqueous extract of licorice root, is known to have various immune-modulating and biological response-modifier activities. GL is used in patients with hepatitis to reduce the activity of liver inflammation; however, the mechanism underlying the anti-inflammatory activity of GL is poorly understood. As antigen-presenting dendritic cells (DC) in the tissue play a major role in the regulation of the inflammatory mucosal milieu during tissue inflammation, we studied whether the function of liver DC was altered by GL therapy in a murine model of concanavalin-A (con A)-induced hepatitis.


METHODS
Liver DC were propagated from control mice or mice with Con-A-induced hepatitis, and the effect of GL on liver DC was evaluated in vivo and in vitro.


RESULTS
The levels of interleukin (IL)-10 produced by liver DC were significantly lower in mice with Con-A-induced hepatitis compared with control mice. However, treatment with GL caused increased production of IL-10 in mice with Con A-induced hepatitis. The increased production of IL-10 by mice with Con A-induced hepatitis was also confirmed in vitro by culturing liver DC with GL.


CONCLUSIONS
This study indicates that increased production of IL-10 by liver DC due to GL administration may be involved in downregulation of the levels of liver inflammation in mice with Con A-induced hepatitis. Glycyrrhizin (GL), an aqueous extract of licorice root, is known to have various immune-modulating and biological response-modifier activities. GL is used in patients with hepatitis to reduce the activity of liver inflammation; however, the mechanism underlying the anti-inflammatory activity of GL is poorly understood. As antigen-presenting dendritic cells (DC) in the tissue play a major role in the regulation of the inflammatory mucosal milieu during tissue inflammation, we studied whether the function of liver DC was altered by GL therapy in a murine model of concanavalin-A (Con A)-induced hepatitis.
Abe
Masanori
M
Third Department of Internal Medicine, Ehime University School of Medicine, 791-0295, Ehime, Shigenobu-cho, Japan.
Akbar
Fazle
F
Hasebe
Aki
A
Horiike
Norio
N
Onji
Morikazu
M
D000410:Alanine Transaminase / Q000097:blood / Q000187:drug effects; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000008:administration & dosage*; D015415:Biomarkers / Q000097:blood; D003208:Concanavalin A / Q000008:administration & dosage; D003713:Dendritic Cells / Q000187:drug effects* / Q000378:metabolism*; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005802:Genes, MHC Class II / Q000187:drug effects; D019695:Glycyrrhizic Acid / Q000008:administration & dosage*; D006505:Hepatitis / Q000378:metabolism*; D007274:Injections, Intraperitoneal; D016753:Interleukin-10 / Q000378:metabolism*; D018664:Interleukin-12 / Q000378:metabolism; D008099:Liver / Q000166:cytology* / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D010641:Phenotype; D012965:Sodium Chloride / Q000494:pharmacology; D006377:T-Lymphocytes, Helper-Inducer / Q000187:drug effects / Q000378:metabolism; D013997:Time Factors
D000894:Anti-Inflammatory Agents, Non-Steroidal; D015415:Biomarkers; D003208:Concanavalin A; D016753:Interleukin-10; D018664:Interleukin-12; D012965:Sodium Chloride; D019695:Glycyrrhizic Acid; D000410:Alanine Transaminase