Abstract

Glycyrrhizae Radix (GR) is a Korean traditional herb medicine that is widely used in clinical health care. Glycyrrhetic acid (GA) is an aglycone saponin extracted from GR that has anti-inflammatory, anti-cancer, and anti-viral effects. However, the anti-inflammatory effects of GA in colitis have not been reported. This study investigated the role of GA on ulcerative colitis in a dextran sulfate sodium (DSS)-induced mouse colitis model. DSS-treated mice displayed weight loss and shortened colon length compared with control mice. Mice administered GA showed less weight loss and longer colon length than the DSS-treated group. Interleukin (IL)-6, IL-1β, and tumor necrosis factor-alpha were decreased by GA treatment. GA treatment also reduced DSS-induced microscopic damage to colon tissue. GA regulates the phosphorylation of transcription factors including nuclear factor-kappa B (NF-κB) and IκB alpha, and regulates the expression of cycloxygenase-2 and prostaglandin E2. GA thus showed beneficial effects in a mouse model of colitis, implicating GA might be a useful herb-derived medicine in the treatment of ulcerative colitis.

Highlights

  • Ulcerative colitis (UC) is a chronic and relapsing inflammatory disease characterized by dysregulation of the immune function response and imbalanced release of cytokines and unresolved inflammatory progress associated with intestinal mucosa [1,2]

  • The results suggest that the anti-inflammatory effect of of Glycyrrhetic acid (GA) is attributable to the regulation of COX-2 in Dextran sulfate sodium (DSS)-induces colitis

  • We found that GA reduced reduced epithelial injury and inflammatory cell infiltration into colon tissue

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Summary

Introduction

Ulcerative colitis (UC) is a chronic and relapsing inflammatory disease characterized by dysregulation of the immune function response and imbalanced release of cytokines and unresolved inflammatory progress associated with intestinal mucosa [1,2]. Patients with bowel disease have increased interleukin (IL)-6 in the intestinal mucosa and tumor necrosis factor-alpha (TNF-α) in the blood and colon tissue. Immune cells, such as T cells, intestinal epithelial cells, and macrophages, secrete various cytokines including TNF-α, IL-1 family, IL-6, IL-8, and interferon-gamma (IFN-γ), which regulate the inflammatory response in UC. GAcan canreduce reducethe theoxidative oxidativestress stresscaused causedby bycarbon carbon tetrachloride, reduces production of pro-inflammatory cytokines, and repress immune function tetrachloride, reduces production of pro-inflammatory cytokines, and repress immune function[15] These results suggest that has inhibitory effects on DSS-induced colitis model.

Results
Effects of GA on Inflammatory Cytokines Level in DSS-Induced UC
10. Values
Effects of GA on Transcription Factors in DSS-Induced UC
Effects of GA on Epithelial Injury in DSS-Induced UC on on Epithelial
Values
Effects
Discussion
Reagents
DSS-Induced UC
Western Blot Analysis
Histological Processing
Conclusions
Full Text
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