adenosine/inflammation

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N6 -(2-hydroxyethyl)-adenosine from Cordyceps cicadae protects against diabetic kidney disease via alleviation of oxidative stress and inflammation.

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This study investigated the kidney-protective ability of N⁶ -(2-hydroxyethyl)-adenosine (HEA) in alloxan-induced diabetic rats. Diabetes was induced in the rats by the administration of alloxan monohydrate (150 mg/kg, i.p) and treated with HEA for 6 weeks. Diabetic rats displayed marked

Adenosine receptors: new therapeutic targets for inflammation in diabetic nephropathy.

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Diabetes is one of the risk factors to human health, which progressively leads to renal complications known as diabetic nephropathy. Many previous studies illustrated biochemical and morphological abnormalities in various animal models of diabetic nephropathy, which may be attributed to altered

Evaluation of Serum Adenosine Deaminase and Inflammatory Markers in Psoriatic Patients.

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Adenosine deaminase (ADA) is an enzyme involved in purine metabolism and it is a marker of nonspecific T-cell activation. Few studies have shown high levels of ADA in the epidermis and sera of psoriatic patients. Other inflammatory markers such as high-sensitive C-reactive protein

Adaptation to inflammatory acidity through neutrophil-derived adenosine regulation of SLC26A3.

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Acute intestinal inflammation includes the early accumulation of neutrophils (PMN). Based on recent evidence that PMN infiltration "imprints" changes in the local tissue environment through local oxygen depletion and the release of adenine nucleotides, we hypothesized that the interaction

AMP-activated protein kinase agonist N6-(3-hydroxyphenyl)adenosine protects against fulminant hepatitis by suppressing inflammation and apoptosis.

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Both AMP-activated protein kinase (AMPK) agonist and inhibitor have been reported to protect against fulminant hepatitis, implying that AMPK may play a complicated role in the development of fulminant hepatitis. In this study, we exploited whether the novel AMPK agonist N6-(3-hydroxyphenyl)adenosine

Anti-inflammatory activity of non-nucleoside adenosine deaminase inhibitor FR234938.

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Adenosine has anti-inflammatory activity. Adenosine deaminase (EC 3.5.4.4) metabolizes extracellular adenosine, resulting in an exacerbation of inflammation. Consequently, it was hypothesized that adenosine deaminase inhibitors produce anti-inflammatory activity by increasing extracellular adenosine

Adenosine in inflammatory joint diseases.

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Inflammatory joint diseases are a group of heterogeneous disorders with a variety of different etiologies and disease manifestations. However, there are features that are common to all of them: first, the recruitment of various inflammatory cell types that are attracted to involved tissues over the

Platelet hyper-reactivity in active inflammatory arthritis is unique to the adenosine diphosphate pathway: a novel finding and potential therapeutic target.

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OBJECTIVE To assess the influence of disease activity on platelet function in patients with inflammatory arthritis (IA). METHODS Ninety-six patients with an established diagnosis of IA (RA, PsA, seronegative SpA) were recruited. Patients with a history of cardiovascular disease (CVD), diabetes

Anti-inflammatory, antioxidant, and antiparkinsonian effects of adenosine A2A receptor antagonists.

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The purpose of the study was to examine derivatives of annelated xanthines (imidazo-, pyrimido-, and diazepino-purinediones) for potential anti-inflammatory effects in carrageenan-induced paw edema in mice. Additionally, their antioxidant activity using the FRAP (ferric-reducing ability of plasma)

Adenosine-mediated bronchoconstriction and lung inflammation in an allergic mouse model.

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In this study, we studied the role of adenosine on airway responsiveness and airway inflammation using an allergic mouse model. Mice were sensitized by two i.p. injections of ragweed and three consecutive ragweed aerosol challenges. It was found that inhalation of adenosine causes a dose-related

Involvement of A1 adenosine receptors in altered vascular responses and inflammation in an allergic mouse model of asthma.

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Poor lung function and respiratory disorders like asthma have a positive correlation with the development of adverse cardiovascular events. Increased adenosine levels are associated with lung inflammation that could lead to altered vascular responses and systemic inflammation. We hypothesized that

Involvement of mast cells in adenosine-mediated bronchoconstriction and inflammation in an allergic mouse model.

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In allergen-induced asthma, activation of lung mast cells leads to bronchial constriction, increased mucus secretion, and an increase in the localization of inflammatory cells to the airways. The purpose of this study was to explore the role of mast cells in adenosine-mediated airway reactivity and

Enhanced airway reactivity and inflammation in A2A adenosine receptor-deficient allergic mice.

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A(2A) adenosine receptor (A(2A)AR) has potent anti-inflammatory properties, which may be important in the regulation of airway reactivity and inflammation. Inflammatory cells that possess A(2A)AR also produce nitrosative stress, which is associated with pathophysiology of asthma, so we hypothesized

Adenosine-mediated alteration of vascular reactivity and inflammation in a murine model of asthma.

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Chronic respiratory disorders such as asthma are believed to be associated with adverse cardiovascular events. We hypothesize that asthmatic inflammation translates into systemic inflammation and alters vascular responses where adenosine (AD) plays an important role. Therefore, this study

Effects of adenosine receptor antagonists on the in vivo LPS-induced inflammation model of Parkinson's disease.

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The study shows effects of the nonselective adenosine A1/A2A receptor antagonist caffeine and the selective A2A receptor antagonist KW6002 on LPS-induced changes in the extracellular levels of dopamine (DA), glutamate, adenosine, hydroxyl radical, and A2A receptor density in the rat striatum.

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