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Modulation expression of tumor necrosis factor α in the radiation-induced lung injury by glycyrrhizic acid.

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To evaluate the ability of glycyrrhizic acid (GLA) to reduce the tumor necrosis factor α (TNF-α), release on messenger ribonucleic acid (mRNA) and protein production in the lungs using GLA in response to irradiation were studied. The animals were divided into four groups: No treatment (NT group),

Synergistic effect of tolfenamic acid and glycyrrhizic acid on TPA-induced skin inflammation in mice.

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Tolfenamic acid (TA) and glycyrrhizic acid (GA) are well-known components with anti-inflammatory properties. However, their combined effects on inflammation have not been well studied. The present study aimed to investigate the in vivo anti-inflammatory effects of TA combined with GA using a

Ability of Post-treatment Glycyrrhizic Acid to Mitigate Cerebral Ischemia/Reperfusion Injury in Diabetic Mice

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BACKGROUND Diabetes aggravates cerebral ischemia/reperfusion (I/R) injury by increasing inflammatory reactions, but its specific mechanism is currently unclear. MATERIAL AND METHODS Diabetes was induced in mice with a high-fat diet combined with streptozotocin. These mice were subjected to transient

Optimal ratio of 18α- and 18β-glycyrrhizic acid for preventing alcoholic hepatitis in rats.

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The glycyrrhizic acid (GA) epimers 18α- and 18β-GA exert anti-inflammatory and hepatoprotective activities, which may help to protect against alcoholic liver disease, particularly alcoholic hepatitis (AH). The aim of the present study was to investigate the optimal ratio of 18α- and 18β-GA for

Glycyrrhizic acid suppresses inflammation and reduces the increased glucose levels induced by the combination of Porphyromonas gulae and ligature placement in diabetic model mice.

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Diabetic patients are at an increased risk of developing severe and progressive periodontitis. Periodontal disease also increases the severity of diabetes by enhancing insulin resistance. Therefore, the regulation of periodontal inflammation in diabetic patients may contribute to the control of both

Glycyrrhizic acid prevents enteritis through reduction of NF‑κB p65 and p38MAPK expression in rat.

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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

Glycyrrhizic acid and 18β-glycyrrhetinic acid modulate lipopolysaccharide-induced inflammatory response by suppression of NF-κB through PI3K p110δ and p110γ inhibitions.

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The roots and rhizomes of licorice ( Glycyrrhia ) species have been used extensively as natural sweeteners and herbal medicines. The aim of this work was to determine the in vitro anti-inflammatory effects of glycyrrhizic acid (GA) and 18β-glycyrrhetinic acid (18βGA) from licorice in a

Identification of a key candidate gene‑phenotype network mediated by glycyrrhizic acid using pharmacogenomic analysis.

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Glycyrrhizic acid (GA) is primarily used as an anti‑inflammatory agent in cases of chronic hepatitis. However, its underlying mechanisms in diverse biological processes and its reported benefits are yet to be fully elucidated. In the current study, an analytical method based on pharmacogenomics was

Anti-Inflammatory activities of licorice extract and its active compounds, glycyrrhizic acid, liquiritin and liquiritigenin, in BV2 cells and mice liver.

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This study provides the scientific basis for the anti-inflammatory effects of licorice extract in a t-BHP (tert-butyl hydrogen peroxide)-induced liver damage model and the effects of its ingredients, glycyrrhizic acid (GA), liquiritin (LQ) and liquiritigenin (LG), in a lipopolysaccharide

Antioxidative and antiinflammatory activities of asiatic acid, glycyrrhizic acid, and oleanolic acid in human bronchial epithelial cells.

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Protective effects of triterpenic acids, asiatic acid (AA), glycyrrhizic acid (GA), or oleanolic acid (OA), for two human bronchial epithelial cells, 16HBE and BEAS-2B cells, against hydrogen peroxide (H2O2) induced injury were examined. Cells were pretreated by triterpenic acid at 4 or 8 μmol/L and

Glycyrrhizic acid suppresses Cox-2-mediated anti-inflammatory responses during Leishmania donovani infection.

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OBJECTIVE The aim of the present study was to characterize glycyrrhizic acid (GA) and assess its immunomodulatory potential in a model of experimental visceral leishmaniasis. METHODS The antileishmanial activity of GA was tested in an amastigote-macrophage model and its non-cytotoxic dose was

Glycyrrhizic acid activates chicken macrophages and enhances their Salmonella-killing capacity in vitro.

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OBJECTIVE Salmonella enterica remains a major cause of food-borne disease in humans, and Salmonella Typhimurium (ST) contamination of poultry products is a worldwide problem. Since macrophages play an essential role in controlling Salmonella infection, the aim of this study was to evaluate the

Glycyrrhizic acid in the treatment of liver diseases: literature review.

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Glycyrrhizic acid (GA) is a triterpene glycoside found in the roots of licorice plants (Glycyrrhiza glabra). GA is the most important active ingredient in the licorice root, and possesses a wide range of pharmacological and biological activities. GA coupled with glycyrrhetinic acid and

Glycyrrhizic acid ameliorates HMGB1-mediated cell death and inflammation after renal ischemia reperfusion injury.

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BACKGROUND Renal ischemia reperfusion injury (IRI) leads to acute kidney injury (AKI) and the death of tubular epithelial cells (TEC). The release of high-mobility group box-1 (HMGB1) and other damage-associated molecular pattern moieties from dying cells may promote organ dysfunction and

Protective effect of glycyrrhizic acid on cerebral ischemia/reperfusion (I/R) injury via inhibiting HMGB1 mediated TLR4/NF-κB pathway.

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Cerebral ischemia is caused by various disorders, such as stroke, myocardial infarction or peripheral vascular disease. The purpose of this paper was to investigate the effects of glycyrrhizic acid (GA) on cerebral ischemia/reperfusion (I/R) injury. Middle cerebral artery occlusion (MCAO) was

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