carbenoxolone/inflammation

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Carbenoxolone decreases monocrotaline‑induced pulmonary inflammation and pulmonary arteriolar remodeling in rats by decreasing the expression of connexins in T lymphocytes.

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The adaptive immune response mediated by T lymphocytes is a well‑established factor in the pathogenesis of pulmonary inflammation. Changes in the expression of various connexins (Cxs) or disruption of connexin‑mediated cellular communication in T lymphocytes contribute to inflammation or tissue

Carbenoxolone ameliorates hepatic lipid metabolism and inflammation in obese mice induced by high fat diet via regulating the JAK2/STAT3 signaling pathway.

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Carbenoxolone (CBX) is the active principle of licorice, which is used to treat psoriasis, peptic ulcers, and wound healing. However, there is no report on how CBX ameliorates hepatic lipid metabolism and inflammation in obese mice. In this study, our aim is to explore the mechanism by which CBX

Effects of carbenoxolone on alveolar fluid clearance and lung inflammation in the rat.

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OBJECTIVE 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2), which requires oxidized nicotinamide adenine dinucleotide as a cofactor, metabolizes endogenous glucocorticoids. Since 11beta-HSD2 has been detected in lung epithelial cells, we examined whether carbenoxolone, a potent inhibitor of

Local amplification of glucocorticoids by 11beta-hydroxysteroid dehydrogenase type 1 and its role in the inflammatory response.

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Glucocorticoids are widely used to treat chronic inflammatory conditions including rheumatoid arthritis. They promote mechanisms important for normal resolution of inflammation, notably macrophage phagocytosis of leukocytes undergoing apoptosis. Prereceptor metabolism of glucocorticoids by

Controlled trial of a new dosage form of carbenoxolone (Pyrogastrone) in the treatment of reflux esophagitis.

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A new preparation combining carbenoxolone sodium with alginate antacid (Pyrogastrone), taken for 8 weeks, was compared with alginate antacid alone (Gaviscon-like) in a controlled double-blind study in 37 patients with endoscopically proved reflux esophagitis. Complete remission or persistence of

Extracellular ATP mediates inflammatory responses in colitis via P2 × 7 receptor signaling.

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Extracellular purinergic products, particularly ATP, have recently been implicated to regulate immune cell functions and contribute to aberrant inflammatory responses of immune diseases. However, regulation of immune responses of colitis by extracellular ATP and its main receptor, P2 × 7, remains to

Peripheral inflammation augments gap junction-mediated coupling among satellite glial cells in mouse sympathetic ganglia.

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Intercellular coupling by gap junctions is one of the main features of glial cells, but very little is known about this aspect of satellite glial cells (SGCs) in sympathetic ganglia. We used the dye coupling method to address this question in both a prevertebral ganglion (superior mesenteric) and a

Carbenoxolone prevents the development of fatty liver in C57BL/6-Lep ob/ob mice via the inhibition of sterol regulatory element binding protein-1c activity and apoptosis.

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Carbenoxolone is the 3-hemisuccinate of glycyrrhetinic acid, the active principal of licorice (Glycyrrhiza glabra). It was reported that carbenoxolone improved glucose tolerance with increased insulin sensitivity in mice with high fat diet-induced obesity. In the present study, we elucidated the

Post-inflammatory Ileitis Induces Non-neuronal Purinergic Signaling Adjustments of Cholinergic Neurotransmission in the Myenteric Plexus.

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Uncoupling between ATP overflow and extracellular adenosine formation changes purinergic signaling in post-inflammatory ileitis. Adenosine neuromodulation deficits were ascribed to feed-forward inhibition of ecto-5'-nucleotidase/CD73 by high extracellular adenine nucleotides in the inflamed ileum.

Glucocorticoid availability in colonic inflammation of rat.

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Recent in vitro studies have shown the involvement of pro-inflammatory cytokines in the regulation of the local metabolism of glucocorticoids via 11beta-hydroxysteroid dehydrogenase type 1 and type 2 (11HSD1 and 11HSD2). However, direct in vivo evidence for a relationship among the local metabolism

HMGB1-carbenoxolone interactions: dynamics insights from combined nuclear magnetic resonance and molecular dynamics.

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The interplay of protein dynamics and molecular recognition is of fundamental importance in biological processes. Atomic-resolution insights into these phenomena may provide new opportunities for drug discovery. Herein, we have combined NMR relaxation experiments and residual dipolar coupling (RDC)

Formulation of carbenoxolone for delivery to the skin.

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Carbenoxolone (CEX), a semi-synthetic derivative of glycyrrhetinic acid, has previously been used as a disodium salt for the management of dyspepsia and peptic ulcer because of its anti-inflammatory properties. Although glycyrrhetinic acid is available in pharmaceutical and personal care products

Effects of intrathecal carbenoxolone treatment on nociception and analgesia in rat.

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BACKGROUND Gap junctions (GJ) are important in pain signalling at the spinal cord level. OBJECTIVE The aim of this investigation was to study the effects of GJ on nociception and the analgesic/hyperalgesic effects of morphine following administration of carbenoxolone as a GJ blocker. Male Wistar

Early inflammatory responses in experimental cardiac hypertrophy and fibrosis: effects of 11 beta-hydroxysteroid dehydrogenase inactivation.

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In epithelial tissues such as kidney, mineralocorticoid receptors (MR) are protected against glucocorticoid occupancy by the enzyme 11 beta-hydroxysteroid dehydrogenase (11 beta HSD) type 2. If the enzyme is congenitally inactive, or blocked by carbenoxolone, physiologic glucocorticoids act as MR

Mediators of mineralocorticoid receptor-induced profibrotic inflammatory responses in the heart.

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Coronary, vascular and perivascular inflammation in rats following MR (mineralocorticoid receptor) activation plus salt are well-characterized precursors for the appearance of cardiac fibrosis. Endogenous corticosterone, in the presence of the 11betaHSD2 (11beta hydroxysteroid dehydrogenase type 2)

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