title: Glycyrrhizic acid prevents enteritis through reduction of NF‑κB p65 and p38MAPK expression in rat.
abstract: Glycyrrhizic acid has a variety of biological properties, including a protective function in the liver, and anti‑inflammatory, anti‑ulcer, anti‑anaphylaxis, anti‑oxidant, immunoregulatory, antiviral and anticancer activities. The efficacy of glycyrrhizic acid can be increased when combined with other medicines. In the present study, the potential protective effects of glycyrrhizic acid against enteritis in rats, and its role in regulating anti‑inflammation, anti‑oxidation, angiogenic and apoptotic mechanisms were investigated using enzyme‑linked immunosorbent and bicinchoninic acid assays, and reverse transcription‑quantitative polymerase chain reaction and western blotting analyses. Adult male Sprague‑Dawley rats were injected with 20 mg/kg methotrexate (MTX) to establish enteritis. Additionally, rats with MTX‑induced enteritis were peritoneally injected with 200 mg glycyrrhizic acid for 9 weeks. The current study demonstrated that glycyrrhizic acid could alleviate MTX‑induced increases of tumor necrosis factor‑α, interleukin (IL)‑1β and IL‑6 levels, and raise IL‑10 levels, in rats with enteritis. Treatment with glycyrrhizic acid significantly reduced D‑lactate and intercellular adhesion molecule‑1 gene expression (P<0.01), but did not inhibit diamine oxidase activity in MTX‑induced enteritis. Pretreatment with glycyrrhizic acid significantly suppressed the promotion of p38 mitogen‑activated protein kinase (p38MAPK), nuclear factor‑κB p65 (NF‑κB p65) protein expression, interferon‑γ protein concentration, and caspase‑3 and cycloxygenase‑2 activity in MTX‑induced enteritis (P<0.01). The findings of the current study suggest that glycyrrhizic acid may prevent enteritis by reducing NF‑κB p65 and p38MAPK expression levels, which may inform future therapeutic strategies for the treatment of enteritis.
authors.affiliation: Department of Pediatric Surgery, Linyi People's Hospital, Linyi, Shandong 276003, P.R. China.
authors.forename: Yi-Ming
authors.initials: YM
authors.lastname: Wang
authors.affiliation: Department of Pediatric Surgery, Linyi People's Hospital, Linyi, Shandong 276003, P.R. China.
authors.forename: Guo-Qiang
authors.initials: GQ
authors.lastname: Du
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000737:chemistry / Q000494:pharmacology / Q000627:therapeutic use; D015153:Blotting, Western; D053148:Caspase 3 / Q000378:metabolism; D051546:Cyclooxygenase 2 / Q000378:metabolism; D016207:Cytokines / Q000032:analysis; D015536:Down-Regulation / Q000187:drug effects*; D004751:Enteritis / Q000139:chemically induced / Q000188:drug therapy / Q000473:pathology; D004797:Enzyme-Linked Immunosorbent Assay; D019695:Glycyrrhizic Acid / Q000737:chemistry / Q000494:pharmacology* / Q000627:therapeutic use; D018799:Intercellular Adhesion Molecule-1 / Q000235:genetics / Q000378:metabolism; D019344:Lactic Acid / Q000097:blood; D008297:Male; D008727:Methotrexate / Q000633:toxicity; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D051996:Transcription Factor RelA / Q000378:metabolism*; D048051:p38 Mitogen-Activated Protein Kinases / Q000378:metabolism*
chemical_list: D000893:Anti-Inflammatory Agents; D016207:Cytokines; C000609942:ICAM1 protein, rat; D051996:Transcription Factor RelA; D018799:Intercellular Adhesion Molecule-1; D019344:Lactic Acid; D019695:Glycyrrhizic Acid; D052247:Nitric Oxide Synthase Type II; D051546:Cyclooxygenase 2; D048051:p38 Mitogen-Activated Protein Kinases; D053148:Caspase 3; D008727:Methotrexate